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Home , Esophagus, Nerve, Vagus nerve

SURGERY FOR BENIGN DISEASE OF THE UPPER

H. DAVID REINES, M.D. FACS VCU School of Medicine Inova Campus Inova Fairfax Hospital 22

OUTLINE:

• WHAT IS THE UPPER GI TRACT? • OF • BENIGN DISEASE OF THE ESOPHAGUS – Achalasia – Gastro-esophageal Reflux Disease-GERD – Zenker’s Diverticulum

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OUTLINE: ESOPHAGUS-ANATOMY

• – Anatomy Physiology Longitudinal grooves fuse to form TE septum. Disease - PUD Incomplete fusion = TE grows, recanalizes. Zollinger - Ellison syndrome Stress ulcer Striated muscle upper enervated by vagus, in middle supplied by visceral • , position because of unequal PUD growth of greater curve of stomach.

• STOMACH (cont.) [ Left vagus Anterior, right vagus posterior- LARP ]

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1 ESOPHAGUS ANATOMY

Cervical esophagus - Below cricopharyngeus muscle,continuation of pharyngeal constrictors -Potential space posteriorly=Zenkers diverticulum

Cervical esophagus = 5cm - C6-T1 - Recurrent laryngeal nerve in groove esophagus and

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ESOPHAGUS-ANATOMY ESOPHAGEAL ANATOMY

Total length incisors to GE junction:35-40cm • Abdominal esophagus via diaphragmatic hiatus Thoracic esophagus : – Surrounded by phrenoesophageal ligament - Upper part stuck to posterior trachea, courses – Lower esophageal is zone of high right of , then left pressure 3-5 cm long at end of esophagus - Covered only by flimsy mediastinal pleura, – Hiatus is surrounded by right and left crus, a sling sight of Boerhaave’s syndrome (perforation) of muscular fibers Lower esophagus : • Blood supply- segmental - Easiest access through L chest – Cervical- inferior - Good for , fundoplication – Thoracic-bronchial and aorta - Entire esophagus needs right side of chest – Abdominal-left gastric and inferior phrenic 9 10

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ESOPHAGEAL PHYSIOLOGY ESPOHAGEAL PHYSIOLOGY needs to get from the to the stomach. is a once initiated : pushes food down 2-4 cm/s-9 1. The pushes the into the posterior Seconds to distal , the elevates (keeping food esophagus. The lower from going up nose) sphincter opens By 2. covers opening of relaxation coinciding With pharyngeal 3. Pressure in hypopharynx can be 60 mm hg swallow. Alpha 4. Food goes into upper esophagus-closes and Adrenergic transmitters contracts in a peristaltic wave with high closing or beta blockers pressure which prevents reflux stimulate LES. 5. The upper sphincter relaxes 15 16

Lower Esophageal Sphincter Lower Esophageal Sphincter

• INCREASE • DECREASE – , motilin – , – bombesin, estrogen, , B-enkephalin, progesterone, substance P , secretin, – antacids, cholinergics calcitonin, – , neuropeptideY, VIP, PGF2 anticholinegrics, barbiturates, calcium channelblockers, PGe1, E2, theophylline, caffeine,, ethanol, peppermint, 17 18 coffee, fat

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Gastro Esophageal Reflux Disease- GERD • Incidence - 4-7% • Role of H.Pylori - probably not • Clinical - , regurgitation, occasionally • Heartburn = substernal “burning” like chest , worsened by coffee, liquor 1-2 hours post prandial, relieved by antacids, h2 blockers • Regurgitation - spontaneous, esp lying down • Dysphagia - food getting stuck low down

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GERD GERD-manometry normals

• Symptoms only 2/3 diagnostic Parameter median 2.5th % 97.5% • DDX - achalasia, spasm, esophageal , cholelithiasis, , peptic Pressure 13 5.8 27 ulcer, CAD (mmhg) Overall 3.6 2.1 5.6 • Erosive 25-40%, related to length cm severity of heartburn and frequency Abd. 2 0.9 4.7 • Dx - UGI, , manometry, Length Bernstein test cm

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4 HIATAL

• Type I-sliding hiatal • Type II-paraesophageal- - GE junction in GE junction at the chest ,gastric •No hernia sac fundus herniates into chest • Most common • has hernia sac “upside • 50% patients with GERD down stomach-can have sliding HH twist=gastric • Repair-fix crus or pull • Pull stomach into stomach into abdomen, fixate it • Do a wrap • ? Do a wrap

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GERD

• If pressure is low, length is short, or sphincter not in abdomen, increased abdominal pressure can overcome the sphincter and you reflux • Gastric distension greater than 20 mmHg can force open the sphincter. open at lower pressures • Fundic distension from high fat diet causes sphincter to get exposed to .repeated exposure leads to inflammation

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5 GERD

• Process can lead to a Schatzki’s ring-fibrotic mucosal ring at the squamocolumnar junction • Condition in which tubular esophagus is lined with columnar rather than squamous described by in 1950 • Intestinal > 3cm long • Occurs in 7-10 % patients with GERD. Metaplasia-dypsplasia-carcinoma sequence • 5-10% dysplasia converts to dyplasia/year and 1% progress to 31 32

Barretts Esophagus

• Treatment- aggressive esp. if dysplasia-60-80 mg proton pump inhibitor x 3 months • • Follow up frequently • New data – surgery () may cure • High grade dysplasia - 50% chance - esophagogastrectomy - 90% curable

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6 GERD-treatment surgical

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GERD-treatment surgical

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SURGERY for GERD- COMPLICATIONS • - 0.5 % • Temporary swallowing problems 50 % • Dysphagia > 3 months 7 % • Increased flatus 47 % • 44 % • Inability to belch 20 % • Inability to vomit 25 %

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7 GERD-treatment results ACHALASIA

• Surgical results – 87 - 96% negative pH tests at • Absence of esophageal peristalsis and failure of 3 months. 88% patients no or minimal reflux at 5 the LES to completely relax upon swallowing yrs. • Quality of Life all better post-surgery • Loss of myenteric ganglion cells • Cost - med vs. surg - short term medicine/long • Low incidence (most patients in 20-40’s) term surgery • SURGERY WORKS. • Squamous cell Cancer develops in 5% over 20 years • Minimally invasive surgery works well! • WHEN THEY FAIL MEDICAL THERAPY, OPERATE!!!!

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ACHALASIA

• Diagnosis-solid food dysphagia and some liquid dysphagia, esp. cold liquids • Average length symptoms 2 yrs • Regurgitation frequent • X-ray “birds beak” • Endoscopy - dilated esophagus with closed LES, but opens easily for scope • Manometry - incomplete sphincter relaxation

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ACHALASIA ACHALASIA

• Treatment-Pharmacotherapy with smooth • -standard non- muscle relaxants include calcium channel operative therapy. Breaks muscle fibers of blockers, nitrates, . Each reduces LES. Pneumatic dilatation response-60- LES pressure, but do not effect symptoms, don’t 80% work long term • Risk of perforation. Long term ? • toxin-BOTOX- inhibits from presynapse nerve terminals. Injected into • Best results- operative myotomy. Divide LES, decreases tone, effective short term, safe?, muscles, keep mucosa.May need long term-60-80% effective antireflux as well. 2000 CASES,2 ,47-90% SUCCESS

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ESOPHAGEAL DIVERTICULA

• Diverticulum - epithelial lined mucosal pouch that protrudes from the esophageal . Most are acquired. Most are PULSION diverticula because of increased intraluminal pressure forces mucosa to herniate through muscles

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ZENKER’S DIVERTICULUM ZENKER’S DIVERTICULUM

• 1878- Zenker reported 27 cases of • Dx-Barium esophagogram pharyngoesphageal diverticulum. Most • Treatment - relieve the neuromotor common, usually 7th or 8th decade abnormality, lower pressure, manage • Arise within the inferior pharyngeal diverticulum. constrictor, point of traction in posterior pharynx (Killians triangle) • Endoscopic division ? • Sx-cervical dysphagia, regurgitation of • Myotomy and diverticulectomy undigested food, aspiration, gurgling, • Myotomy and diverticulopexy halitosis, voice changes •Myotomy

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9 ESOPHAGUS-other benign diseases1

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SURGERY FOR BENIGN DISEASE OF THE UPPER GASTROINTESTINAL TRACT

H. DAVID REINES, M.D. FACS VCU School of Medicine Inova Campus Inova Fairfax Hospital

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