Hematoxylin and eosin staining of tongue (a and b) and esophagus (c and d). (a and c) Wild-type mouse at 12 months of age. (b and d) L2D1+/p53+/– mouse at 12 months of age. b and d show evidence of nuclear atypia, enlargement, and hyperchromasia of cells as well as loss of polarity with migration of atypical cells into intermediate and superficial layers as cellular and histologic features of dysplasia. In particular, there is invasion of malignant cells into the submucosa and muscle of the tongue and into the submucosa of the esophagus. Cancer lesions are marked by arrows. (e) Hematoxylin and eosin staining and (f) pancytokeratin immunohistochemistry from one representative paraesophageal lymph node metastasis. There are keratin-positive epithelial cells within the lymphatic tissue. Magnification, ×400.
2. 2<br />Esophagus<br />Upper 1/3 is skeletal muscle<br />Lower 1/3 is smooth muscle<br />middle is combo of both<br />Contains two sphincters<br />Lined by squamous epithelium<br />< 3 cm below diaphragm<br />
4. The act of swallowing is comprised of a series of events requiring intact central, autonomic, and enteric nervoussystems as well as a set of functional striated and smooth muscles<br />Interference with these precise mechanisms will result in dysphagia<br />
5. Esophagus<br /><ul><li>Lesions of the esophagus run from bland esophagitis to highly lethal cancers.
6. All produce dysphagia (difficulty in swallowing), which is attributed either to deranged esophageal motor function or to narrowing or obstruction of the lumen.
7. Heartburn or Gastroesophageal reflux disease (GERD)(retrosternal burning pain) usually reflects regurgitation of gastric contents into the lower esophagus.</li></li></ul><li>Less commonly, hematemesis (vomiting of blood) andmelena(blood in the stools) are evidence of severe inflammation, ulceration, or laceration of the esophageal mucosa. <br />Massive hematemesis may reflect life-threatening rupture of esophageal varices. <br />esophageal varices are extremely dilated sub-mucosal veins in the lower esophagus<br />
8. Patho----- Of-------Eso<br />Structural abnormalities of the esophagus can be either congenital or acquired. <br />The two most common congenital esophageal abnormalities are <br />Esophageal Atresia (EA) and<br />Tracheoesophageal Fistula (TEF).<br />Anatomic disorders encountered infrequently (Table). <br />8/5/2011<br />7<br />
9. Selected Anatomic Disorders Of The Esophagus<br />
10. ANATOMIC AND MOTOR DISORDERS <br /><ul><li>Motility Abnormalities</li></ul>Motility abnormalities create difficulty in swallowing, called dysphagia.<br />Dysphagia is a symptom of several esophageal motility disorders as well as several obstructive disorders such as esophageal webs or Schatzkiring: narrowing of the lower part of the esophagus that can cause difficulty swallowing. <br />The narrowing is caused by a ring of mucosal tissue (which lines the esophagus) or muscular tissue.<br />8/5/2011<br />copyright (your organization) 2003<br />9<br />
11. ANATOMIC AND MOTOR DISORDERS <br /><ul><li>Both esophageal anatomy and function may be affected secondarily by many esophageal disorders.
12. In hiatal hernia, separation of the diaphragmatic crura and widening of the space between the muscular crura and the esophageal wall permits a dilated segment of the stomach to protrude above the diaphragm.</li></li></ul><li>Two anatomic patterns are recognized: the axial, or sliding hernia and the nonaxial, or paraesophageal hernia.<br />The sliding hernia constitutes 95% of cases; protrusion of the stomach above the diaphragm creates a bell-shaped dilation, bounded below by the diaphragmatic narrowing.<br />In paraesophageal hernias, a separate portion of the stomach, usually along the greater curvature, enters the thorax through the widened foramen. The cause of this deranged anatomy is obscure. <br />
13. Comparison of the two forms of esophageal hiatal hernias<br />
14. 8/5/2011<br />13<br />
15. <ul><li>Only about 9% of these adults, however, suffer from heartburn or regurgitation of gastric juices into the mouth.
16. These symptoms more likely result from incompetence of the lower esophageal sphincter than from the hiatal hernia and are accentuated by positions favoring reflux (bending forward, lying supine) and obesity.
17. Although most patients with sliding hiatal hernias do not have reflux esophagitis, those with severe reflux esophagitis are likely to have a sliding hiatal hernia.
18. Other complications affecting both types of hiatal hernias include mucosal ulceration, bleeding, and even perforation.
19. Paraesophageal hernias rarely induce reflux, but they can become strangulated or obstructed. </li></li></ul><li>Achalasia<br /><ul><li>Achalasia The term achalasiameans "failure to relax" and in the present context denotes incomplete relaxation of the lower esophageal sphincter in response to swallowing.
20. This produces functional obstruction of the esophagus, with consequent dilation of the more proximal esophagus.
21. Three major abnormalities in achalasia: </li></ul>Aperistalsis(absence of peristalsis )<br />partial or incomplete relaxation of the lower esophageal sphincter with swallowing<br />increased resting tone of the lower esophageal sphincter. <br />
22. <ul><li>It is generally accepted that in primary achalasia there is loss of intrinsic inhibitory innervation of the lower esophageal sphincter and smooth muscle segment of the esophageal body.
23. Secondary achalasia may arise from pathologic processes that impair esophageal function.
24. The classic example is Chagas disease, caused by Trypanosomacruzi, which causes destruction of the myenteric plexus of the esophagus, duodenum, colon, and ureter. </li></li></ul><li>17<br />a: Normal myenteric plexus demonstrating multiple ganglion cells and minimal lymphocytic infiltration. b: Mild myenteric inflammation. There is mild lymphocytic inflammation, and ganglion cells can be identified.<br />c: Moderate myenteric inflammation with lymphocytic infiltrate is present. Ganglion cells are absent. <br />d: Severe myenteric inflammation with lymphocytes densely clustered within this myenteric plexus. Ganglion cells are absent.<br />
25. Morphology<br /><ul><li>In primary achalasia there is progressive dilation of the esophagus above the level of the lower esophageal sphincter.
26. The wall of the esophagus may be normal thickness, thicker than normal because of hypertrophy of the muscularis, or markedly thinned by dilation.</li></li></ul><li>Although achalasia is not a mucosal disease, stasis of food may produce mucosal inflammation and ulceration proximal to the lower esophageal sphincter.<br />Achalasia is characterized clinically by progressive dysphagia and inability to completely convey food to the stomach.<br />Nocturnal regurgitation and aspiration of undigested food may occur. It usually becomes manifest in young adulthood, but it may appear in infancy or childhood.<br />The most serious aspect of this condition is the hazard of developing esophageal squamous cell carcinoma, reported to occur in about 5% of patients and typically at an earlier age than in those without achalasia.<br />
27. Symptoms<br />Backflow (regurgitation) of food<br />Chest pain, which may increase after eating or may be felt in the back, neck, and arms<br />Cough<br />Difficulty swallowing liquids and solids<br />Heartburn <br />Unintentional weight loss<br /><ul><li>Examination </li></ul>Esophageal manometry: is a test used to measure the function of the lower esophageal sphincte by specific tube through esogh to stomach<br />Esophagogastroduodenoscopy <br />Upper GI x-ray <br />20<br />
28. Treatment<br />Incurable<br />Palliative measures<br />Nonsurgical<br />Surgical<br />Both are directed toward relieving the obstruction caused by the no relaxing LES( lower esogh I don’t know)<br />
29. Treatment<br /><ul><li>The approach to treatment is to reduce the pressure at the lower esophageal sphincter.
30. Therapy may involve:
31. Injection with botulinum toxin (Botox). This may help relax the sphincter muscles, but any benefit wears off within a matter of weeks or months.
32. Medications, such as long-acting nitrates or calcium channel blockers, which can be used to relax the lower esophagus sphincter.
33. Surgery(called an esophagomyotomy), which may be needed to decrease the pressure in the lower sphincter.
34. Wideling (dilation or balloon) of the esophagus at the location of the narrowing (done during esophagogastroduodenoscopy).</li></ul>8/5/2011<br />22<br />
35. Lacerations (Mallory-Weiss Syndrome) <br /><ul><li>Longitudinal tears in the esophagus at the esophagogastric junction.
36. The presumed pathogenesis is inadequate relaxation of the musculature of the lower esophageal sphincter during vomiting,
37. with stretching and tearing of the esophagogastric junction at the moment of propulsive expulsion of gastric contents.</li></li></ul><li><ul><li>This thinking is supported by the fact that a hiatal hernia is found in more than 75% of patients with Mallory-Weiss tears.
38. Tears may involve only the mucosa or may penetrate the wall.
39. Infection of the defect may lead to an inflammatory ulcer or to mediastinitis[is inflammation of the tissues in the mid-chest].
40. Esophageal lacerations account for 5% to 10% of upper gastrointestinal bleeding episodes.
41. Most often bleeding is not profuse and ceases without surgical intervention, but life-threatening hematemesis may occur.
42. Even with severe blood loss, supportive therapy with vasoconstrictive medications, transfusions, and sometimes balloon tamponade, is usually required.</li></li></ul><li>Varices<br /><ul><li>When portal venous blood flow into the liver is impeded by cirrhosis or other causes, the resultant portal hypertension induces the formation of collateral bypass channels.
43. The increased pressure in the esophageal plexus produces dilated tortuous vessels called varices.
44. Patients with cirrhosis develop varices at a rate of 5% to 15% per year, so that varices are present in approximately two thirds of all cirrhotic patients. They are most often associated with alcoholic cirrhosis. </li></li></ul><li>8/5/2011<br />26<br />
45. MORPHOLOGY<br /><ul><li>Varices appear primarily as tortuous dilated veins lying primarily within thesubmucosaof the distal esophagus and proximal stomach.
46. The net effect is irregular protrusion of the overlying mucosa into the lumen, although varices are collapsed in surgical or postmortem specimens .
47. When the varixis unruptured, the mucosa may be normal, but often it is eroded and inflamed because of its exposed position, further weakening the tissue support of the dilated veins.
48. Esophageal varices: a view of the everted esophagus and gastroesophageal junction, showing dilated submucosal veins (varices). The blue-colored varices have collapsed in this postmortem specimen.</li></li></ul><li>Note the markedly dilated veins in the submucosa and in the muscularispropria of the esophagus.<br /><ul><li>These dilated varices often cause pressure atrophy and ulceration of the overlying mucosa, as has happened in this case.
49. The subsequent inflammation of the submucosa causes erosion of the thin wall of the varices with subsequent rupture.
50. The large varix noted by the arrow communicates directly with the lumen and has probably ruptured in the past. </li></li></ul><li>29<br />Shows thrombosis of a large submucosalvarix.<br /> Note the ulceration of the overlying mucosa (arrow) and inflammation of the esoph. <br />
51. <ul><li>The factors leading to initial rupture of a varix are unclear: increased tension in progressively dilated veins, and vomiting with increased intra-abdominal pressure are likely to be involved.
52. Once begun, variceal hemorrhage subsides spontaneously in only 50% of cases; endoscopic injection of thrombotic agents (sclerotherapy) or balloon tamponade is often required.
53. When varices bleed, 20% to 30% of patients die during the first episode.
54. Among those who survive, rebleeding occurs in approximately 70% within 1 year, with a similar rate of mortality for each episode.</li></li></ul><li>ESOPHAGITIS<br /><ul><li>Injury to the esophageal mucosa with subsequent inflammation is a common condition worldwide. The inflammation may have many origins: prolonged gastric intubation, uremia, ingestion of corrosive or irritant substances, and radiation or chemotherapy.
55. There are many presumed contributory factors:
56. Decreased efficacy of esophageal antireflux mechanisms
57. Inadequate or slowed esophageal clearance of refluxed material
58. The presence of a sliding hiatal hernia
59. Increased gastric volume, contributing to the volume of refluxed material
60. Impaired reparative capacity of the esophageal mucosa by prolonged exposure to gastric juices
61. Any one of these influences may assume primacy in an individual case, but more than one is likely to be involved in most instances.</li></li></ul><li>MORPHOLOGY<br />The anatomic changes depend on the causative agent and on the duration and severity of the exposure. <br />Mild esophagitis may appear macroscopically as simple hyperemia, with virtually no histologic abnormality.<br />In contrast, the mucosa in severe esophagitis exhibits confluent epithelial erosions or total ulceration into the submucosa.<br />Three histologic features are characteristic of uncomplicated reflux esophagitis, although only one or two may be present:<br />(1) eosinophils, with or without neutrophils, in the epithelial layer;<br />(2) basal zone hyperplasia; and (3) Elongation of lamina propria papillae. Intraepithelial neutrophils are markers of more severe injury.<br />
62. 33<br />Reflux esophagitis showing the superficial portion of the mucosa. Numerous eosinophils(arrows) are present within the mucosa, and the stratified squamous epithelium has not undergone complete maturation owing to ongoing inflammatory damage.<br />
63. 8/5/2011<br />34<br />
64. Clinical Features<br /><ul><li>The dominant manifestation of reflux disease is heartburn, sometimes accompanied by regurgitation of a sour brash.
66. Chest pain, particularly behind the breastbone, that occurs with eating Swallowed food becoming stuck in the esophagus (food impaction).
67. Rarely, chronic symptoms are punctuated by attacks of severe chest pain mimicking a heart attack.
68. Although largely limited to adults older than age 40, reflux esophagitis is occasionally seen in infants and children.
69. The potential consequences of severe reflux esophagitis are bleeding, development of stricture, and Barrett esophagus, with its predisposition to malignancy.</li></li></ul><li>BARRETT ESOPHAGUS <br /><ul><li>Barrett esophagus is a complication of long-standing gastroesophageal reflux, occurring in up to 10% of patients with persistent symptomatic reflux disease, as well as in some patients with asymptomatic reflux.
70. Barrett esophagus is defined as the replacement of the normal distal stratified squamous mucosa by metaplastic columnar epithelium containing goblet cells.
71. Prolonged and recurrent gastroesophageal reflux is thought to produce inflammation and eventually ulceration of the squamous epithelial lining.
72. Healing occurs by in growth of stem cells and re-epithelialization.
73. In the microenvironment of an abnormally low pH in the distal esophagus caused by acid reflux, the cells differentiate into columnar epithelium.</li></li></ul><li>MORPHOLOGY<br /><ul><li>Barrett esophagus is apparent as a salmon-pink, velvety mucosa between the smooth, pale pink esophageal squamous mucosa and the more lush light brown gastric mucosa.
74. Microscopically, the esophageal squamous epithelium is replaced by metaplastic columnar epithelium (gastric mucosa ).
75. Critical to the pathologic evaluation of patients with Barrett mucosa is the recognition ofdysplasticchanges in the mucosa that may be precursors of cancer.</li></li></ul><li>8/5/2011<br />38<br />Barrett esophagus. <br />A, Endoscopic view showing red velvety gastrointestinal-type mucosa extending from the gastroesophageal orifice. Note paler squamous esophageal mucosa. <br />B, Microscopic view showing mixed gastric- and intestine-type columnar epithelial cells in glandular mucosa.<br />
76. <ul><li> Barrett esophagus affects males more often than females (ratio of 4:1) and is much more common in whites than in other races. Genetic factors are suggested by clustering in families.
77. Ulcer and stricture may develop as a complication of Barrett esophagus. However, the chief clinical significance of Barrett esophagus relates to the development of adenocarcinoma.
78. Patients with Barrett esophagus have a 30- to 40-fold greater risk of developing esophageal adenocarcinoma compared with normal populations.</li></li></ul><li>8/5/2011<br />40<br />Normal gastric mucosa<br />
79. ESOPHAGEAL CARCINOMA <br /><ul><li>Benign tumors may arise in the esophagus from both the squamous mucosa and underlying mesenchyme. However, these are overshadowed by cancer of the esophagus, of which there are two types: squamous cell carcinomas and adenocarcinomas.
80. Worldwide, Squamous cell carcinomas constitute 90% of esophageal cancers.
81. Adenocarcinoma arising in Barrett esophagus is more common in whites than in blacks. By contrast, squamous cell carcinomas are more common in blacks worldwide.
82. There are striking and puzzling differences in the geographic incidence of esophageal carcinoma. In the United States, there are about 6 new cases per 100,000 population per year.
83. In regions of Asia extending from the northern provinces of China to Iran, the prevalence is well over 100 per 100,000. </li></li></ul><li>Etiology and Pathogenesis <br /><ul><li>The environmental and dietary factors associated with squamous cell carcinoma.
84. An important contributing factor is retarded passage of food through the esophagus, prolonging mucosal exposure to potential carcinogens such as those contained in tobacco and alcoholic beverages.
85. There is a well-defined predisposing role for chronic esophagitis, itself associated with alcohol and tobacco.
86. The role of genetic predisposition is extremely ill defined, but the rare genetic syndrome of tylosis,
87. characterized by excess keratin formation in the skin of the palm and soles, carries an almost certain probability of the development of esophageal cancer.</li></li></ul><li>RISK FACTORS FOR SQUAMOUS CELL CARCINOMA OF THE ESOPHAGUS<br /><ul><li>Esophageal Disorders
93. Deficiency of vitamins (A, C, riboflavin, thiamine, pyridoxine)
94. Deficiency of trace metals (zinc, molybdenum)
95. Fungal contamination of foodstuffs
96. High content of nitrites/nitrosamines
97. Genetic Predisposition
98. Tylosis (hyperkeratosis of palms and soles)</li></li></ul><li>MORPHOLOGY<br /><ul><li>Squamous cell carcinomasare usually preceded by a long prodrome of mucosal epithelial dysplasia followed by carcinoma in situ and, ultimately, by the emergence of invasive cancer.
99. Early overt lesions appear as small, gray-white, plaque like thickenings or elevations of the mucosa. In months to years, these lesions become tumorous, taking one of three forms:
100. (1) polypoidexophytic masses that protrude into the lumen;
101. (2) Necrotizing cancerous ulcerations that extend deeply and sometimes erode into the respiratory tree, aorta, or elsewhere; and
102. (3) diffuse infiltrative neoplasms that impart thickening and rigidity to the wall and narrowing of the lumen. Whichever the pattern, about 20% arise in the cervical and upper thoracic esophagus, 50% in the middle third, and 30% in the lower third. </li></ul>Large ulcerated squamous cell carcinoma of the esophagus<br />Exophytic<br />growing outward<br />
104. 46<br /><ul><li>The epithelial lining above is clearly abnormal compared to the normal single-layer ciliated epithelium below.
105. There is nuclear stratification, nuclear enlargement, hyperchromasia, pleomorphism, and mitoses.
106. The photomicrograph above shows pseudoinvasion but the same architectural and cytological features.
107. Deeper levels from the block from which the above photomicrograph was taken shows continuity with the surface epithelium. proliferation activity in serous carcinoma:</li></li></ul><li>47<br />Micrograph of an esophageal adenocarcinoma (dark blue - upper-left of image) and normal squamous epithelium (upper-right of image). H&E stain.<br />Histology of squamous cell carcinoma element of the esophageal tumor. Keratinization is seen. (b) Small cell carcinoma element of the esophageal carcinoma. The tumor cells shows characteristic morphologies of small cell carcinoma.<br /> (c) Adenocarcinoma element of the esophageal carcinoma. Tubular formations are seen. There is a gradual transition between adenocarcinoma element and small cell carcinoma element. (d) Transitional zone between squamous cell carcinoma element and small cell carcinoma element of the esophageal carcinoma. <br />
108. 8/5/2011<br />copyright (your organization) 2003<br />48<br />Microscopic Image of Esophageal Squamous Cell Carcinoma<br />Microscopic image of Squamous Papilloma of the Esophagus<br />
109. <ul><li>Adenocarcinomas appear to arise from dysplastic mucosa in the setting of Barrett esophagus.
110. Unlike squamous cell carcinomas, they are usually in the distal one third of the esophagus and may invade the subjacent gastric cardia.
111. Initially appearing as flat or raised patches on an otherwise intact mucosa, they may develop into large nodular masses or exhibit deeply ulcerative or diffusely infiltrative features.
112. Microscopically, most tumors are mucin-producing glandular tumors exhibiting intestinal-type features, in keeping with the morphology of the preexisting metaplastic mucosa.
113. The occasional development of tumors of other alimentary cell types supports the concept that Barrett epithelium arises from multipotential cells.</li></li></ul><li>Clinical Features<br /><ul><li>Esophageal carcinoma is insidious in onset and produces dysphagia and obstruction gradually and late.
114. Weight loss, anorexia, fatigue, and weakness appear, followed by pain, usually related to swallowing. Diagnosis is usually made by imaging techniques and endoscopic biopsy.
115. Because these cancers extensively invade the rich esophageal lymphatic network and adjacent structures, surgical excision rarely is curative.
116. Thus, there is emphasis on routine screening procedures, particularly for those with manifestations of chronic esophagitis or known Barrett esophagus.
117. Esophageal cancer detected when confined to the mucosa or submucosa is amenable to surgical treatment.</li></li></ul><li>Gastroesophageal reflux disease (GERD)<br />Gastroesophageal reflux (GER) is defined as passage of gastric contents into the esophagus.<br /> GER is a normal physiologic process that occurs throughout the day in healthy infants, children, and adults. <br />Gastroesophageal reflux disease (GERD) occurs when gastric contents reflux into the esophagus or oropharynx and produce symptoms.<br />Regurgitation is defined as passage of refluxed gastric contents into the oral pharynx. <br />Vomiting is defined as expulsion of the refluxed gastric contents from the mouth. <br />8/5/2011<br />51<br />
118. Definitions<br />
119. Causes<br /><ul><li>When you eat, food passes from the throat to the stomach through the esophagus (also called the food pipe or swallowing tube).
120. Once food is in the stomach, a ring of muscle fibers prevents food from moving backward into the esophagus.
121. These muscle fibers are called the lower esophageal sphincter, or LES</li></ul>8/5/2011<br />53<br />
124. 8/5/2011<br />copyright (your organization) 2003<br />56<br /><ul><li>The esophageal biopsy specimen at center, from a patient with GER, shows a small number of intraepithelial eosinophils.
125. Basal cell thickening of the esophageal mucosal epithelium and lengthening of stromal papillae, also depicted, are additional markers of GER.
126. If biopsy reveals extensive eosinophilia, for example, >20 intraepithelial eosinophils per high-power microscopic field (HPF), an allergic condition or idiopathic esophagitis, rather than GER, should be considered.
127. The histologic picture at right is of primary eosinophilic esophagitis, showing clusters of eosinophils and papillary and basal increases; this patient had dysphagia and food allergies that responded to an elimination diet.
128. Normal esophagus (left); GER (center), with approximately 5 eosinophils per HPF; and primary eosinophilic esophagitis (right)</li></li></ul><li>GastroesophagealReflux<br />-<br />Developmental delay<br />Upright posture<br />Esophageal peristalsis <br />Saliva production<br />-<br />-<br />+<br />Esophagitis<br />+<br />Acid in Esophagus<br />Cough, RAD<br />reactive airways disease<br />+<br />+<br />Increased gastric outlet pressure<br />Decreased LES pressure<br />
129. Symptoms<br /><ul><li>A burning sensation in your chest (heartburn), sometimes spreading to the throat, along with a sour taste in your mouth
130. Chest pain
131. Difficulty swallowing (dysphagia)
132. Hoarseness or sore throat
133. Regurgitation of food or sour liquid (acid reflux)
134. Sensation of a lump in the throat</li></ul>8/5/2011<br />58<br />
135. Respiratory Symptoms of GER<br />Apnea/ALTE<br />Stridor and hoarseness<br />Cough<br />Wheezing<br />Recurrent pneumonia<br />
136. Diagnosis<br /><ul><li>Esophagoscopy
137. To note mucosal changes
138. Esophageal biopsies
139. To note changes at the cellular level
140. Motilitiy studies
141. Low LES pressures are associated with reflux
142. pH monitoring
143. The most precise measure for the presence of acid in the esophageal lumen (24 hour monitoring)</li></li></ul><li><ul><li>Esophagogastroduodenoscopy and biopsy provide information about the severity of GERD.
144. The presence of inflammation in the esophagus suggests significant peptic injury, whereas inflammation in the stomach or duodenum may support other conditions, such as food allergy.</li></ul>8/5/2011<br />copyright (your organization) 2003<br />61<br />Diagnosis<br />
145. Medical Treatment<br />
146. Surgical Treatment<br /><ul><li>Indications for surgical treatment are somewhat controversial
147. Stage 0 and Stage 1 disease should never be an indication for surgery
148. Stage 2 disease should always undergo a well supervised period of medical management for at least six months to a year
149. Stage 3 disease should also undergo medical therapy first
150. In stage2 and in Stage 3 disease surgical options should be entertained after failed medical management</li></li></ul><li>Surgical Treatment<br /><ul><li>Nissen fundoplication
151. Total or partial
152. Their aim is to:
153. Restore normal anatomy (intra-abdominal segment of esophagus)
154. Re-creating an appropriate high-pressure sound at the esophagogastric junction
155. Maintaining this repair in the normal anatomic position</li></li></ul><li>