Ben Degner Dave Yonick October 26th, 2011

Ben Degner Dave Yonick October 26th, 2011
GERD/Barrett's Esophagus, Dysphagia, Hiatal Hernia, and Laparoscopic Antireflux Procedure Ben Degner Dave Yonick October 26th, 2011

Anatomy Mucosa, submucosa, muscularis propria, and adventitia
Lack serosa vs. other GI tract Mucosa innermost (4 layers) contains squamous epithelium

Muscularis Propria Continuation of inferior constrictor of the pharynx
Two muscle bundles inner circular outer longitudinal Striated upper 1/3 -vagus and its recurrent laryngeal branches Smooth lower 2/3 -visceral nerve plexus derived from neural crest cells Left vagus anterior-liver/biliary tree Right vagus posterior-celiac plexus

Esophageal Arteries Upper-Inferior Thyroid Artery
Lower-Left Gastric and Inferior Phrenic arteries, bronchial arteries and 4-6 aortic branches

Esophageal Veins

Esophageal Lyphatics Lymphatics: upper 2/3 cephalad, lower 1/3 caudad

Anatomy

Anatomic Areas of Narrowing
Cricopharyngeal muscle Left mainstem bronchus and aortic arch Diaphragm

Anatomic Areas of Narrowing

UES 15 cm from incisors Cricophayrngeus muscle, recurrent laryngeal nerve Site of perforation is cricopharyngeus muscle (with EGD), aspiration if UES fail

LES 40 cm from incisors No anatomic landmarks
rise in pressure when transducer is pulled from the stomach Increased Pressure: Alpha-adrenergics, BBs, gastrin, motilin, antacids, cholinergics, metoclopramide Decreased Pressure: Alpha blockers, Beta andrenergics, CCK, estrogen, glucagon, progesterone, somatostatin, secretin, barbiturates, CCBs, caffeine, diazepam, dopamine, meperidine, ethanol, coffee, fat

LES High pressure except:
1. passage of food into the stomach 2. when fundus is distended with gas, LES eliminated to allow venting of the gas Loss of the normal high-pressure zone leads to GERD (transient vs permanent)

Gastroesophageal Reflux Disease
1/3 Western population experience symptoms at least once a month 4-7% daily Most patients with mild symptoms carry out self-medication The prevalence and severity of GERD is increasing

Typical GERD Symptoms Heartburn Regurgitation Dysphagia
substernal burning or chest pain worse with spicy foods, tomato sauce, citrus juices, chocolate, coffee, and alcohol 1 to 2 hours after eating, often at night, relieved by antacids and OTC H2 blockers Regurgitation sensation that fluid or food is returning into the esophagus worse at night or when lying down after a meal Dysphagia up to 40% of pts with GERD have sensation of food hanging up in the lower esophagus--esophageal dysphagia typically limited to only solid food, with normal passage of liquids, suggesting mechanical disorder develops slowly enough that the patient may adjust eating habits unknowingly

Atypical GERD Symptoms
Cough, asthma, hoarseness, and noncardiac chest pain primary complaint in 20-25% more difficult to prove a cause-and-effect relationship trial of high-dose PPIs is helpful make sure patient doesn’t have another cause for pain

Pathophysiology of GERD
Fundic distention because of overeating LES is taken up by the expanding fundus, exposing the squamous epithelium/LES to gastric juice Worsened by delayed gastric emptying with high-fat diet and hiatal hernia Compensated with increased swallowing Saliva bathe the injured mucosa and alleviate the discomfort = aerophagia, bloating, repetitive belching More distension leads to further exposure and repetitive injury to the terminal squamous epithelium leading to inflammation continued epigastic pain and possibly epithelial columnarization Extension of the inflammatory process into the muscularis propria leading to a permanently defective sphincter

Diagnosis of GERD Based on symptoms alone?
Correct in only 2/3 of patients these symptoms are not specific for GE reflux achalasia, diffuse spasm, esophageal carcinoma, pyloric stenosis, cholelithiasis, gastritis, gastric or duodenal ulcer, and coronary artery disease need objective diagnosis before the decision is made for surgical treatment

Diagnosis of GERD First episode
Initial therapy with H2 blockers or PPI for 12 weeks Failure of H2 blockers or PPI to control the symptoms suggests that either the diagnosis is incorrect or the patient has severe disease EGD Opportunity for assessing the severity of mucosal damage 24-hour pH and bilirubin monitoring Measurement degree and pattern of esophageal exposure to gastric and duodenal juice Manometry Assess the status and function of the LES and esophageal body These studies identify features that predict a poor response to medical therapy, frequent relapses, and the development of complications

Complications of GERD Mucosal complications-esophagitis and stricture
Extraesophageal or Respiratory complications, such as laryngitis, recurrent pneumonia, and progressive pulmonary fibrosis Reflux (aspiration) vs reflex (vagal bronchoconstriction) Metaplastic and Neoplastic complications, Barrett's and esophageal adenocarcinoma Prevalence/severity of complications related to the degree of loss of the GE barrier and content of refluxed gastric juice, not symptoms

Barrett’s Esophagus Squamous epithelium metaplasia  columnar epithelium 7-10% of patients with GERD Normally, the SCJ should coincide with the GEJ (linear gastric mucosal folds) Presence of any columnar mucosa extending at least 3 cm into the esophagus (goblet cells)=Barrett’s predisposed to malignant degeneration Increased risk of adenocarcinoma x50

Classification and Management of Barrett’s Esophagus with Dysplasia
Indefinite for Dysplasia: Aggressive antireflux therapy (60 mg PPI per day) and repeated biopsy in 3 months Low Grade: Aggressive antireflux therapy vs. surgical treatment High Grade-Esophagectomy and PPI

Dysphagia Difficulty in transferring a food from the mouth to the stomach Regurgitation, chest pain, heartburn, and coughing or choking spells Oropharyngeal functional disturbance in the swallowing mechanism Esophageal mechanical obstruction or esophageal motility disorder

Dysphagia Evaluation of a patient with dysphagia must be performed in a systematic manner Barium swallow Additional diagnostic tests EGD, manometry, 24-hour pH study, and possibley bronchoscopy and endoscopic ultrasonography (EUS). Diagnostic imaging by CT and PET in assessing patients with esophageal cancer

Oropharyngeal Dysphagia
inability to chew food, drooling, coughing during a meal, and nasal regurgitation of solids or liquids dysphagia within 1 second of swallowing The common causes can be grouped into three broad categories: 1) generalized systemic conditions: CVA, Myasthenia gravis 2) intrinsic functional disturbances: Zenker's diverticulum 3) fixed mechanical obstruction: Neoplasm, webs, previous surgical treatment, previous radiation therapy

Esophageal Dysphagia Dysphagia with solids? =Mechanical Obstruction
Intermittent? Esophageal Ring or Esophagitis Progressive with GERD? Peptic Stricture Progressive with weight loss and anorexia? Esophageal Cancer Dysphagia for both liquids and solids? =Motility Disorder Intermittent? Spasm (DES) Progressive with GERD? Scleroderma Progressive? Achalasia

Schatzki's Ring symmetrical narrowing at SCJ, small hiatal hernia
correlation with GERD barium swallow and esophagoscopy to confirm Asymptomatic? no specific treatment is needed Definitive treatment? dilatation of the ring with medical therapy for GERD. If refractory, dilatation plus antireflux surgery

Peptic Stricture greater length and more tapered than Schatzki’s
H/o GERD worsening dysphagia for years without weight loss End stage of ulcerative esophagitis, healing ulcer causes annular fibrosis Dx: barium swallow followed by upper GI endoscopy greater length and more tapered than Schatzki’s

Esophageal Webs localized narrowing of the esophagus caused by intraluminal extension of the mucosa and part of the submucosa congenital or acquired (mc), usually secondary to conditions such as iron deficiency anemia/Plummer-Vinson syndrome and ulcerative colitis. Tx: endoscopic dilatation

Achalasia Dysphagia for liquids and solids and possibly weight loss.
Barium swallow shows absent peristalsis and a dilated esophagus, possibly tapered narrowing in distal esophagus=bird's beak Achalasia risk factor for squamous cell cancer Tx: Pneumatic dilatation or surgery

Diffuse esophageal spasm
unknown etiology Nonprogressive dysphagia with solids and liquids and nonexertional chest pain that responds to nitroglycerin corkscrew on barium The diagnosis by manometry periodic occurrence of simultaneous high-amplitude contractions with intervening periods of normal peristalsis. Tx: r/o CAD, then medical management of reassurance, nitrates, and CCBs Botulinum toxin injection, surgery does not have an established role

Nutcracker Esophagus unknown etiology women>men
Manometry: peristaltic waves with significantly elevated amplitude (> 180 mm Hg). Treatment is primarily medical

Hypertensive LES unknown etiology
can occur alone or in association with achalasia, nutcracker esophagus, or DES Manometry-LES pressure over 45 mm Hg Tx: primarily medical, but balloon dilatation is done

Esophageal Diverticula
< 5% of all cases of dysphagia. False diverticula (pulsion) include only the mucosal layer underlying motor dysfunction True diverticula (traction) include all layers of the esophageal wall inflammatory process Esophageal diverticula may also be classified into three categories on the basis of the anatomic level at which they occur

Pharyngoesophageal/Zenker’s Diverticula
MC from muscle incoordination that leads to herniation of the mucosa in prox esophagus Dysphagia mc symptom, halitosis, regurgitation, throat discomfort, palpable neck mass, recurrent aspiration pneumonia The best initial diagnostic tool is a barium swallow perforation in EGD

Midesophageal diverticula
True traction diverticula Caused by periesophageal inflammation in granulomatous inflammation of the subcarinal lymph nodes from TB or fungal infection Frequently asymptomatic and are often found incidentally Dysphagia does occur but is a rare symptom

Epiphrenic diverticula
Acquired pulsion diverticula of distal esophagus Associated with other esophageal motor disorders (achalasia, DES, and hypertensive LES) but can occur alone Absent or mild symptoms? Conservative management is appropriate Significant dysphagia? Surgical management

Chemical Ingestion Alkali household cleaning agents
Most occur accidentally in children, but suicide in adults Magnitude and site of the injury? Related to the length of the contact time Injury at any level, MC is distal esophagaus lead to submucosal scar formationstricture and dysphagia Endoscopic exam is first step A barium swallow should be done in the first month after injury to detect any stricture and then serial swallows

Hiatal Hernia I-Sliding, dilation of hiatus, most commonly associated with GERD -most with reflux have sliding, most with sliding don’t have reflux II-Paraesophageal, defect in diaphragm alongside esophagus with normal GE junction --chest pain, dysphagia, early satiety III-Combined I and II IV-entire stomach in chest plus another organ (colon, spleen)

Laparoscopic Antireflux Procedure
Most commonly performed procedure is a fundoplication Nissen Fundoplication: 360 degree fundoplication Laparoscopic approach reduces postoperative pain and shortens length of hospital stay Rapid increase in surgical treatment of GERD

Preoperatively h/o recurrent heartburn enough to clinically establish GERD and initiate empiric medical therapy Those patients with recurrent or refractory symptoms require further evaluation prior to surgery Endoscopy Evaluate for Barrett’s Esophagus Manometry Evaluate for other causes of esophageal dysmotility 24 hour pH May be helpful, especially in those patients with atypical GERD symptoms or other GI comorbidities

Indication Failure of maximal medical therapy
Short 2 month trial Failure of lifestyle modification Weight loss Alteration in diet (avoid chocolate, peppermint, fat, onions, garlic, alcohol, caffeine, nicotine) Avoid food 2-3 hours prior to sleep Elevation of head of bed 6 – 10 inches Limit potentially precipitating activities (bending over or strenuous exercise) Complications of GERD Esophagitis, stricture, recurrent aspiration or pneumonia, Barrett’s esophagus Associated with paraesophageal hernia Intolerance to medical therapy or patient desiring discontinueation of medical therapy

Contraindication Absolute Relative
Inability to tolerate general anesthetic or laparoscopy Uncorrectable coagulopathy Relative Previous upper abdominal surgery Morbid obesity Severe esophagitis with or without stricture Small-body habitus Short esophagus Particularly for fundoplications Paraesophageal hiatal hernia

Basic tenets of antireflux surgery
Restoration of an effective LES Creation of a gastroesophageal valve Mechanical effects of a fundoplication Fundus exhibits a physiologic phenomenon of receptive relaxation Decreased tone of the gastric fundic smooth muscle in association with swallowing-induced relaxation of the LES

Laparoscopic Port Placement

Belsey Mark IV Repair Transthoracic repair to control GERD
Typically performed through a left thoracotomy May be performed thoracoscopically McKernan and Champion modified Belsey Distal esophagus and proximal stomach are mobilized and ddelivered through the esophageal hiatus Anterior 270 degree plication of the fundus is performed onto the esophagus The fundoplication is buttressed by the diaphragmatic crura

Nissen Fundoplication
360 degree wrap around esophagus Circumferentially dissecting the distal esophagus Mobilizing the gastric fundus Plicating the fundus around the lower esophagus Creating a high-pressure zone Increases the resting tone of the sphincter mechanism Improves its response to elevated intragastric pressure Fundoplication varied from 3 – 6 cm and included the esophageal wall in the fundoplication No division of the short gastric vessels

Rossetti-Hell modification
Included wrapping the anterior portion of the fundus around the esophagus No division of the short gastric vessels Minimal moblization of the upper stomach Created a 3 – 6 cm 360 degree fundoplication

Short, floppy Nissen Most common modification used today
The short gastric vessels are divided Full fundic mobilization and the lateral border of the fundus is wrapped around the esophagus Sutured to the medial edge of the medial fundus Short fundoplication, < 2.5 cm Fashioned over a 50 to 60F bougie

Complication of total fundoplication
Dysphagia Inability to belch Gas-bloat syndrome Hypercontinent

Partial Fundoplication
Indication Poor esophageal clearance because of esophageal motility abnormality Severe aerophagia, daytime reflux associated with belching Insufficient gastric fundus Previous gastrectomy Tubular stomach Psychological inability to tolerate side effects of fundoplication Association with Heller myotomy for achalasia

Watson fundoplication
Dor Fundoplication 180 to 200 degree anterior wrap Used in association with Heller esophagomyotomy for achalasia Watson fundoplication Plication of the fundus along the left anterolateral border of the esophagus More physiologic 120 degree anterolateral wrap Toupet fundoplication Most common partial fundoplication laparoscopically 270 degree posterior wrap Fundus pulled posterior to esophagus with suture of leading edge to right anterior aspect of the esophagus

Hill Repair Indication
Reflux symptoms refractory to medical management Younger patients asymptomatic but requiring high-dose medication Avoid lifetime dependence on medication Chronic esophagitis, inflammatory shortening of the esophagus and paraesophageal hernia

Advantage Posterior fixation of GE junction
Prevent recurrent herniation and improve distal esophageal clearance by improving longitudinal function Distal high-pressure zone can be calibrated; avoiding late dysphagia Does not require a gastroplasty with a short esophagus Can be preformed in patients that have undergone a gastrectomy Shorter hospital stay and faster recovery compared to open procedure

Contraindication Morbid obesity Failed previous antireflux operation
Prior extensive upper abdominal surgery

Pre-operative Endoscopy Manometry 24 hour pH study
Evaluate for Barrett’s esophagus Evaluate and grade gastroesophageal valve Grade I: normal musculomucosal valve Grade II: valve that is slightly less defined and shorter than Grade I Grade III: valve is poorly defined; stays open, allows reflux and is associated with a hiatal hernia Grade IV: no definition to the musculomucosal fold; stays open constantly and is associated with a hiatal hernia Manometry Evaluate for Motility disorder 24 hour pH study Evaluate and confirm the diagnosis of GERD

Hill Repair A 43F bougie is passed through the GE junction along with a manometry probe during the repair. Intraoperative manometry is performed to calibrate the GE junction Reconstructed LES is approximately 3 to 4 cm Peak pressure during pull through > 45 mm Hg than sutures are loosened Peak pressure < 20 mm Hg, sutures are tightened Following calibration; sutures are fixed permanently over a bougie Fundus is secured to the rim of the diaphragm Accentuate the angle of His and elongate the gastroesophageal flap valve

Failed Fundoplication
Learning curve requires 30 to 50 operations Decreasing operative time Diminishing rates of complications Dysphagia Excessively tight closure of the esophageal hiatus Tight wrap or tension on the wrap Sliding hiatal hernia with wrap in abdomen Migration of the wrap into the mediastinum Most common complication New-onset substernal or epigastric pain Slipped Nissen Secondary to disruption or migration of the wrap onto the stomach

Questions A 55-year-old man with chronic gastrointestinal reflux undergoes upper endoscopy and is found to have a 4-cm segment of Barrett’s esophagus. Biopsy of the lesion is positive for low-grade dysplasia. Current surveillance recommendations include four-quadrant biopsies every: A) 3 months B) 6 months C) 9 months D) 12 months E) 24 months

A 55-year-old man with chronic gastrointestinal reflux undergoes upper endoscopy and is found to have a 4-cm segment of Barrett’s esophagus. Biopsy of the lesion is positive for low-grade dysplasia. Current surveillance recommendations include four-quadrant biopsies every: A) 3 months B) 6 months C) 9 months D) 12 months-every 2 cm along the length of the Barrett’s segment E) 24 months

A 47-year-old woman has acid reflux that has not responded to therapy with proton pump inhibitors. Her body mass index (BMI) is 43 and she is hypertensive and diabetic. Upper endoscopy reveals grade 1 esophagitis. Esophageal manometry shows good progression of peristalsis with normal lower esophageal sphincter (LES) tone and relaxation. The procedure MOST likely to help this patient overall would be: A) total fundoplication B) partial fundoplication C) gastric bypass D) endoscopic antireflux procedure E) vertical banded gastroplasty

A) total fundoplication
B) partial fundoplication C) gastric bypass D) endoscopic antireflux procedure E) vertical banded gastroplasty -GERD is seen in up to 72% of obese persons -GERD is usually only one of many co-morbidities in obese: OSA, HTN, DM, HL -Fundoplication directed solely at treating GERD does not adequately address the underlying cause, nor does it do anything to help with the other co-morbid conditions -A bariatric procedure allows for weight loss and improvement or resolution of other associated Conditions including GERD

A 42-year-old man has had a long history of gastroesophageal reflux disease (GERD). He has attempted many medication trials, with only minimal relief. A recent endoscopy revealed grade II esophagitis. He is considering surgery. Which of the following studies should be performed before performing a laparoscopic fundoplication? A. Barium swallow B. Esophageal manometry C. Ambulatory pH monitoring D. All of the above

A 42-year-old man has had a long history of gastroesophageal reflux disease (GERD). He has attempted many medication trials, with only minimal relief. A recent endoscopy revealed grade II esophagitis. He is considering surgery. Which of the following studies should be performed before performing a laparoscopic fundoplication? A. Barium swallow B. Esophageal manometry C. Ambulatory pH monitoring D. All of the above -All candidates for a laparoscopic Nissen fundoplication should undergo a preoperative evaluation that includes symptomatic evaluation, barium swallow, endoscopy, esophageal manometry, and ambulatory pH monitoring. -Ambulatory pH monitoring is the most reliable test for the diagnosis of GERD; it has a sensitivity and specificity of about 92%.

A 60 year-old otherwise healthy man has symptomatic GERD that has not responded to medical therapy, including PPIs. Esophagoscopy shows moderately severe esophagitis. Multiple biopsies of the esophageal mucosa in the area of esophagitis show columnar epithelium replacing the normal squamous epithelium. As the patient’s treatment is being planned, a biopsy report shows high-grade dysplasia. Treatment should be: Continued medical treatment with yearly esophagoscopy and biopsies Laparoscopic Nissen fundoplication Photodynamic therapy Esophagectomy Laser ablation of normal mucosa

Four years ago, a 47 year-old woman had a laparoscopic fundoplication
Four years ago, a 47 year-old woman had a laparoscopic fundoplication. It failed after three years and she had severe, recurrent gastroesophageal symptoms. Through a celiotomy incision, the surgeon performed a redo-fundoplication with a 360-degree, 2 cm wrap around a 56 Fr dilator. For the past three months she has had severe early satiety, postprandial epigastric pain, and weight loss. The most likely cause of these symptoms is: A. The wrap is too tight B. The wrap is too loose C. Vagal injury D. Irritable bowel syndrome E. Esophageal motor disorder With injury to the vagus, pts have gastric stasis resulting in retention of food within the stomach for several hours. This may be accompanied by a feeling of fullness and occasionally abdominal pain. In rarer cases, it may be associated with a functional gastric outlet obstruction.

A) will usually regress after Nissen fundoplication
Barrett’s esophagus: A) will usually regress after Nissen fundoplication B) carries an increased risk of squamous cell carcinoma C) is an indication for esophagectomy D) should be followed by endoscopic surveillance E) is a contraindication to laparoscopic Nissen fundoplication Injured squamous cells in the distal esophagus can be replaced either by more squamous cells or, through the process of metaplasia, by columnar cells (Barrett’s esophagus). Chronic gastroesophageal reflux both injures the squamous epithelium and provides the abnormal esophageal environment that stimulates repair through columnar cell metaplasia. Up to three different types of columnar epithelia can be found in Barrett’s esophagus: (1) specialized intestinal metaplasia, which has a villiform surface and intestinal-type crypts lined by mucus-secreting columnar cells and goblet cells; (2) gastric fundic-type epithelium; and (3) junctional-type epithelium. Specialized intestinal metaplasia is the most common, and dysplasia and carcinoma in Barrett’s esophagus are almost invariably associated with specialized intestinal metaplasia. Diagnosis Barrett’s esophagus is more common in men than in women, with a 3:1 male predominance (the average age at diagnosis is 55 years). Barrett’s esophagus and severe GERD are uncommon in blacks. The prevalence of Barrett’s esophagus increases with age up to 70 years. Barrett’s esophagus often remains stable, and no conclusive evidence indicates that either ongoing severe reflux or effective treatment of reflux alters the progression of Barrett’s esophagus despite the association with cancer. The extent of intestinal metaplasia is related to the status of the LES and the degree of esophageal acid exposure.[205] Barrett’s esophagus can be found in 10% to 15% of patients who have endoscopic examinations for symptoms of GERD. Most patients with Barrett’s esophagus do not seek medical attention for esophageal symptoms and may have no symptoms of GERD. GERD associated with Barrett’s esophagus, however, often is severe, with esophageal ulceration, stricture, and hemorrhage. Barrett’s esophagus has been identified in approximately 1 in 10 persons with erosive esophagitis and 1 in 3 persons with a peptic esophageal stricture. In one study, small areas of specialized columnar epithelium with intestinal metaplasia were identified histologically in the region of the gastroesophageal junction in 18% of patients undergoing endoscopy. This finding indicates that “short segment Barrett’s esophagus” may be common in the general population. Whether short-segment Barrett’s esophagus represents a substantial risk factor for esophageal adenocarcinoma is not yet clear. Cancer registries in the United States document that the rate of increase in the frequency of adenocarcinoma of the distal esophagus and gastric cardia exceeds that for any other type of cancer. Most of these tumors arise from Barrett’s epithelium, a finding suggesting that the prevalence of specialized intestinal metaplasia that predisposes to adenocarcinoma is far more common in the general population than had been appreciated. Carcinogenesis in Barrett’s esophagus may involve activation of proto-oncogenes, dysfunction of tumor suppressor genes, or both. Molecular studies have shown that genomic abnormalities in Barrett’s esophagus result in the loss of heterozygosity in a variety of tumor suppressor genes including 17P (encoding p53), 5Q (APC, MCC), 18Q (DCC), and 13Q (RBI). Tumor suppressor genes (p53, P16), oncogenes (c-erbB-2, H-ras, K-ras, cyclin D1, and src), and growth factors or receptors (transforming growth factor-α, epidermal growth factor receptor) are implicated in the 1143 malignant transformation of Barrett’s esophagus and may soon serve as prognostic indicators. Notably, the degree of angiogenesis is not a significant prognostic indicator of esophageal cancer. Flow cytometry has also been used to detect aneuploidy in Barrett’s esophagus. True dysplasia in Barrett’s esophagus represents a neoplastic alteration of the columnar epithelium and is widely regarded as the precursor of invasive malignancy. Unfortunately, dysplasia is not an ideal biomarker of malignant potential in Barrett’s epithelium for several reasons. The histologic interpretation of dysplasia is largely subjective, and the natural history of dysplasia is not clear. Dysplastic Barrett’s mucosa often is indistinguishable from nondysplastic mucosa, and small foci of dysplasia can be easily missed. Despite limitations, dysplasia remains the best biomarker for evaluating malignancy in Barrett’s esophagus. Approximately one third of patients with high-grade dysplasia in Barrett’s esophagus either already have or will develop invasive cancer within several years. The prevalence of adenocarcinoma at the time of diagnosis of Barrett’s esophagus is approximately 8%. The high incidence of esophageal adenocarcinoma has led to the recommendation that all patients with Barrett’s esophagus undergo prospective screening for the development of dysplasia and carcinoma. Although this approach seems reasonable, the benefits of screening in Barrett’s esophagus have not been proven by a prospective clinical trial.

A 47-year-old woman presents with a 1- to 2-month history of postprandial, mild epigastric pain on swallowing solid food. The x-rays shown are obtained. What is the diagnosis and which of the following is appropriate for this patient? A) Esophageal lengthening procedure B) Observation C) Partial gastrectomy D) Stamm gastrostomy E) Surgical reduction

A 47-year-old woman presents with a 1- to 2-month history of postprandial, mild epigastric pain on swallowing solid food. The x-rays shown are obtained. Which of the following is appropriate for this patient? A) Esophageal lengthening procedure B) Observation C) Partial gastrectomy D) Stamm gastrostomy E) Surgical reduction of the hernia -the chest x-ray suggests a paraesophageal hernia

What indicate(s) presence of hiatal hernia?
A) Distal esophageal web B) Cervical esophageal web C) Both D) Neither

What indicate(s) presence of hiatal hernia?
A) Distal esophageal web B) Cervical esophageal web C) Both D) Neither Distal esophageal web, or Schatzki’s ring, is an annular constriction of the esophagus that indicates the presence of a sliding hiatal hernia. Plummer-Vinson syndrome is cervical esophageal dysphagia associated with iron-deficiency anemia. The condition is commonly associated with cervical esophageal webs. Plummer-Vinson syndrome is considered a premalignant condition; 10% of patients develop SCC of hypopharynx, oral cavity, or esophagus. Treatment: of correction of iron deficiency and dilation of cervical webs

Gastroesophageal reflux disease increases risk developing of:
A) Adenocarcinoma of the esophagus B) Squamous cell carcinoma of the esophagus C) Both D) Neither

Gastroesophageal reflux disease increases risk developing of:
A) Adenocarcinoma of the esophagus B) Squamous cell carcinoma of the esophagus C) Both D) Neither -SCC related to lye ingestion, achalasia and EtOH and tobacco -Adenocarcinoma now MC esophageal cancer, related to GERD

Regarding the anatomy of the esophagus:
A) the cervical esophagus lies to the right of the midline B) the thoracic esophagus is anterior to the aortic arch C) the left vagus nerve passes posterior to the esophagus D) the cervical esophagus is supplied by the inferior thyroid artery E) the abdominal esophagus is supplied by the right gastric artery

Ben Degner Dave Yonick October 26th, 2011

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