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Surgery 2020 Git SURGERY 2020 GIT OESOPHAGUS The oesophagus begins at the lower margin of the cricopharyngeous muscle and is approximately 25cm long. It is composed of striated muscle in upper third, smooth muscle in the lower two thirds, and is lined throughout by squamous epithelium. In the mediastinum, the oesophagus is closely related to the two trunks of the vagus nerve, the trachea, the aorta and the heart. Barium swallow may show a slight constriction approximately 2cm above the diaphragm, below which is an area of dilatation known as the vestibule, or phrenic ampulla. The oesophagus enters the stomach approximately 40-45 cm from the incisor teeth. The barrier functions of the oesophagus depend on the upper cricopharyngeal and lower oesophageal sphincters, a zone of high pressure (15- 35 mmHg) extending over lowest 3-4cm of the esophagus; it has no anatomical counterpart. The pH within the oesophagus is usually 5-7, unless there is reflux of acidic gastric contents. A pH of less than 4 is normally considered pathological; assessment is best made by continuous 24 hour pH monitoring. At the gastro-oesophageal junction, the transition from oesophageal to gastric mucosa is easily seen as an irregular circumferential line known as the ora serrata, gastric rosette, or Z-line. Esophageal Diverticula Zenker's diverticulum occurs due to increased pressure in the oropharynx during swallowing against a closed upper esophageal sphincter. Zenker diverticula are an acquired pulsion-type of diverticula that form in the posterior hypopharynx from a defect in the muscular wall, between the inferior pharyngeal constrictor muscle and the cricopharyngeal sphincter (Killian triangle). Retention of undigested food in large diverticula occasionally results in regurgitation, nocturnal cough, and aspiration pneumonia. Imaging Studies: On chest x-rays and CT scans, large diverticula of the esophagus and hypopharynx may also manifest as air or fluid-filled structures communicating with the esophagus. Diagnosis of Zenker diverticulum is made best by barium swallow. Medical Care: In many patients with mid esophageal and epiphrenic diverticula, dysphagia is related to underlying dysmotility; thus, treatment should be directed to the motility disorder when feasible e.g. it can be treated with pneumatic dilation, botulinum toxin injection into lower esophageal sphincter, or surgical Heller esophagomyotomy. Surgical Care: Treatment of Zenker diverticulum is surgical; Surgical options include diverticulectomy with cricopharyngeal myotomy, diverticular suspension (diverticulopexy) with cricopharyngeal myotomy, and cricopharyngeal myotomy alone. Surgical Treatment: o Diverticulectomy & Dohlman's procedure 1 SURGERY 2020 Diverticulectomy Fascia at anterior border of sternomastoid is divided Pouch is identified anterior to prevertebral fascia Pouch is then excised an defect closed Cricopharyngeal myotomy is performed to prevent recurrence Patient is fed via a nasogastric tube for a week postoperatively Complications include: Recurrent laryngeal nerve palsy Cervical emphysema Mediastinitis Cutaneous fistula Dohlman's procedure Is an endoscopic procedure A double-lipped oesophagoscope is used Wall between the diverticulum and oesophageal wall is exposed Hypopharyngeal bar divided with diathermy or laser Barium esophagram, AP Zenker diverticulum, lateral Barium swallow show residual view, demonstrating a view pool of contrast within the bilobed Zenker diverticulum pouch Gastroesophageal Reflux Disease Pathophysiology: The lower esophageal sphincter (LES) must have normal length and pressure and a normal number of episodes of transient relaxation,. The gastroesophageal junction must be located in the abdomen so that the diaphragmatic crura can assist the action of the LES functioning as an extrinsic sphincter. The presence of a hiatus hernia disrupts this synergistic action and can promote reflux. Esophageal clearance must be able to neutralize the acid refluxed (mechanical clearance is by esophageal peristalsis; chemical clearance is due to saliva). The stomach must empty properly. A functional (frequent transient LES relaxation) or mechanical problem of the LES (hypotensive LES) is the most common cause of GERD. Certain foods (coffee, alcohol), medications (calcium channel blockers, nitrates, β blockers), or hormones (progesterone) can decrease LES pressure. Obesity is a contributing factor. History: Typical symptoms include the following: Heartburn/ Regurgitation/ Dysphagia: Atypical symptoms include the following: Cough and/or wheezing/ Hoarseness/ Chest pain: 2 SURGERY 2020 Imaging Studies: 1: Barium esophagogrm: It is particularly important for patients who experience dysphagia. 2: Esophagogastroduodenoscopy: It identifies the presence and severity of esophagitis and the possible presence of Barrett esophagus and also excludes the presence of other diseases that can present similarly, such as a peptic ulcer. Other Tests: 3: Esophageal manometry This study defines the function of the LES and esophageal body (peristalsis). 4: Ambulatory 24-hour pH monitoring This test is the criterion standard for diagnosis of GERD, with a sensitivity of 96% and a specificity of 95%. 5: Radionuclide measurement of gastric emptying Medical Care: Lifestyle modifications include the following: Lose weight (if overweight). Avoid alcohol, chocolate, citrus juice, and tomato-based products. Avoid large meals. Wait 3 hours after a meal before lying down. Elevate head of bed 8 inches. Pharmacological therapy Antacids. Histamine-2 receptor antagonists. Proton pump inhibitors: used only when GERD has been objectively documented. Prokinetic agents: Surgical Care: Indications for fundoplication include the following: Patients with symptoms incompletely controlled by proton pump inhibitor. The presence of Barrett esophagus is an indication for surgery. Presence of extraesophageal manifestations of GERD may indicate the need for surgery. These include (1) respiratory manifestations (cough, wheezing, aspiration); (2) ear, nose, and throat manifestations (hoarseness, sore throat, otitis media); and (3) dental manifestations (enamel erosion). Complications: Esophagitis: The squamous epithelium responds to acid by summoning lymphocytes and neutrophils to the sub-epithelial layers. The resulting mucosal damage and loss of the surface squamous cells then promotes frank ulceration, fibrosis and stricture formation. Barrett's esophagus: The alterations in the lower esophagus, caused by chronic regurgitation of gastric contents, are now recognized to predispose to the development of an adenocarcinoma of the lower esophagus. This risk of malignancy is related to the tendency of the squamous mucosa of the esophagus to be replaced by migrating columnar cells from the upper stomach (cardia). The gastric-type mucosa, placed 3 SURGERY 2020 under considerable stress in its new environment, responds by developing numerous goblet cells, acquiring the characteristics of intestinal tissue, the so called intestinal metaplasia. It is commonly called Barrett's epithelium and has the propensity, over several years, to evolve into a true dysplasia and, eventually, to an adenocarcinoma. The risk of developing Barrett's esophagus is related to the history of regular symptoms of gastro- esophageal reflux, the advancing age (> age 50) and the presence of inflammation of the squamous epithelium related to acid reflux. Risk of malignancy due to intestinal metaplasia of the columnar lined lower esophagus is 30 to 125 times that in the esophagus without the Barrett's changes. When dysplasia does develop, resection of the lower esophagus and a gastric pull-up or jejunal interposition is indicated. Non-surgical eradication of Barrett's Esophagus: Laser ablation of the unwanted columnar intestinal metaplasia can be accomplished in 60-80 %. Fig1: Gastroesophageal reflux disease/Barrett esophagus/adenocarcinom a sequence Fig2: Laparoscopic Nissen fundoplication Hiatal hernia Types: Sliding hiatal hernia (99%) Paraesophageal hernia (1%) congenitally short esophagus (not a true hernia) Associated with: diverticulosis (25%); Gallstones (18%); esophagitis (25%); Duodenal ulcer (20%) (Saint’s triad: Hiatus hernia + diverticulosis + Gall stones) Sliding hiatal hernia "Axial hernia," "concentric hernia": 99% Portion of peritoneal sac forms part of wall of hernia, gastroesophageal junction and a portion of the stomach are above the diaphragm. incidence: increases with age etiology: rupture of phrenicoesophageal membrane due to repetitive stretching. Findings: UGI: Epiphrenic bulge/ distance between B ring and hiatal margin > 2cm/ tortuous esophagus/ gastroesophageal reflux/ 6 thick gastric folds within suprahiatal pouch CT: Dehiscence of diaphragmtic crura > 15 mm/ pseudomass within/above distal esophagus/ fat (omemtum) surrounding distal esophagus 4 SURGERY 2020 Paraesophageal hiatal hernia "Rolling hiatal hernia," "parahiatal hernia" 1% of hiatal hernias. portion of stomach superiorly displaced into the thorax with the esophagogastric junction remaining in the subdiaphragmatic position Findings: The gastroesophageal junction is in the normal location, but a portion of the stomach is adjacent to the esophagus i.e. cardia in normal position herniation of portion of the stomach anterior to esophagus frequently nonreducible, may be associated with gastric ulcer of lesser curvature at level of diaphragmatic hiatus Symptoms and Signs Most patients are asymptomatic, but chest pain can occur. GERD occurs
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