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Esophageal Disorders PowerPoint Presentation

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Description : Check out this medical presentation on Barretts Esophagus, which is titled "Esophageal Disorders", to know about Esophageal Anatomy and Esophageal Disorders.

Tags : Digestive System, Esophageal Disorders, Anatomy, Barretts Esophagus

Published on : Jul 10, 2021 | Views : 4345 | Downloads : 37

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Slide 1-

Esophageal Disorders Dr. Salem M. Bazarah, MD, M.Ed, FACP, FRCPC, FRCPC(GI) & PhD Ass. Prof. & Consultant Gastroenterologist, Hepatologist & Interventional Endoscopist King Abdul Aziz University Director, Liver Transplant Program & Department of Internal Medicine DSFH
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Esophageal Disorders Motility Anatomic & Structural Reflux Infectious Neoplastic Miscellaneous
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Esophageal Anatomy Upper Esophageal Sphincter (UES) Lower Esophageal Sphincter (LES) Esophageal Body (cervical & thoracic) 18 to 24 cm
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Normal Phases of Swallowing Voluntary oropharyngeal phase – bolus is voluntarily moved into the pharynx Involuntary UES relaxation peristalsis (aboral movement) LES relaxation
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Normal Phases of Swallowing Between swallows UES prevents air entering the esophagus during inspiration and prevents esophagopharyngeal reflux LES prevents gastroesophageal reflux peristaltic and non-peristaltic contractions in response to stimuli capacity for retrograde movement (belch, vomiting) and decompression
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Normal Swallowing Cortical Swallowing Areas Swallowing Center Motor Nuclei Oropharynx & Esophagus Frontal cortex Brainstem
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Esophageal Motility Disorders
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Motility Disorders upper esophageal UES disorders neuromuscular disorders esophageal body achalasia diffuse esophageal spasm nutcracker esophagus nonspecific esophageal dysmotility LES achalasia hypertensive LES primary disorders achalasia diffuse esophageal spasm nutcracker esophagus nonspecific esophageal dysmotility secondary disorders severe esophagitis scleroderma diabetes Parkinson’s stroke
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Diagnostic Tools cineradiology or videofluoroscopy (MBS) barium esophagram esophageal manometry endoscopy
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Normal Manometry
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Motility Disorders Based on Manometry Achalasia – Inadequate LES relaxation Diffuse Esophageal Spasm – Uncoordinated contraction Nutcracker Esophagus – Hypercontraction Ineffective Esophageal Motility – Hypocontraction
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Achalasia
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Achalasia first clinically recognized esophageal motility disorder described in 1672, treated with whale bone bougie term coined in 1929 epidemiology 1-2 per 200,000 population usually presents between ages 25 to 60 male=female Caucasians > others average symptom duration at diagnosis: 2-5 years
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Pathophysiology Degeneration of NO producing inhibitory neurons loss of ganglionic cells in the myenteric plexus (distal to proximal) vagal fiber degeneration underlying cause: unknown autoimmune? (antibodies to myenteric neurons in 50% of patients) that affect relaxation of LES Basal LES pressure rises
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Mechanical End Result dual disorder LES fails to appropriately relax resistance to flow into stomach not spasm of LES but an increased basal LES pressure often seen (55-90%) loss of peristalsis in distal 2/3 esophagus
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Clinical Presentation clinical presentation solid dysphagia 90-100% (75% also with dysphagia to liquids) post-prandial regurgitation 60-90% chest pain 33-50% pyrosis 25-45% weight loss nocturnal cough and recurrent aspiration
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Diagnostic Work Up plain film (air-fluid level, wide mediastinum, absent gastric bubble, pulmonary infiltrates) barium esophagram (dilated esophagus with taper at LES) Bird peak good screening test (95% accurate) endoscopy (rule out GE junction tumors, esp. age>60) esophageal manometry (absent peristalsis,  LES relaxation, & resting LES >45 mmHg)
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Manometric Features Incomplete LES relaxation Elevated resting pressure (>45 mmHg) Aperistalsis of esophageal body
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Treatment of Achalasia
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Goals reduce LES pressure and increase emptying
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Nitrates and Calcium Channel Blockers Isosorbide dinitrate Reduces LES Pressure 66% for 90 min Nifedipine Reduces LES pressure 30-40% for > 60 minutes 50-70% initial response; <50% at 1 year limitations: tachyphylaxis and side-effects
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Botulinum Toxin prevents ACH release at NM junction 90% initial response; 60% at 1 year Needs repetitive sessions
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Pneumatic Dilatation Balloon dilatation to 300 psi disrupt circular muscle 60-95% initial success; 60% at 5 years recent series suggest 20-40% will require re-dilation Success increases with repeat dilatations risk of perforation 1-13% (usually 3-5%); death 0.2-0.4%
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Surgical Treatment surgical myotomy (open or minimally-invasive) >90% initial response; 85% at 10 years; 70% at 20 years (85% at 5 years with min. inv. techniques) <1% mortality; <10% major morbidity 10-25% acutely develop reflux, up to 52% develop late reflux
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Spastic Motility Disorders of the Esophagus
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Spastic Motility Disorders of the Esophagus Diffuse Esophageal Spasm Nutcracker Esophagus Hypertensive LES Nonspecific Esophageal Dysmotility
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Epidemiology Any age (mean 40 yrs) Female > Male
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Clinical Presentation Dysphagia to solids and liquids intermittent and non-progressive present in 30-60%, more prevalent in DES (in most studies) Chest Pain constant % across the different disorders (80-90%) swallowing is not necessarily impaired can mimic cardiac chest pain Pyrosis (20%) and IBS symptoms (>50%) Symptoms and Manometry correlate poorly
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Diffuse Esophageal Spasm frequent non-peristaltic contractions simultaneous onset (or too rapid propagation) of contractions in two or more recording leads occur with >30% of wet swallows (up to 10% may be seen in “normals”)
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Nutcracker Esophagus high pressure peristaltic contractions avg pressure in 10 wet swallows is >180 mm Hg 33% have long duration contractions (>6 sec) may inter-convert with DES
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Hypertensive LES Nonspecific Esophageal Dysmotility high LES pressure >45 mm Hg normal peristalsis often overlaps with other motility disorders abnormal motility pattern fits in no other category non-peristalsis in 20-30% of wet swallows low pressure waves (<30 mm Hg) prolonged contractions
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Diagnosis of Spastic Motility Disorders of the Esophagus Manometry Barium Esophagram Endoscopy PH monitoring
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Spastic Motility Disorders of the Esophagus treatment reassurance nitrates, anticholinergics, hydralazine - all unproven calcium channel blockers - too few data with negative controlled studies in chest pain psychotropic drugs – trazodone, imipramine and setraline effective in controlled studies dilation - anecdotal reports, probable placebo effect
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Manometry in Esophageal Symptoms Non-Cardiac Chest Pain Dysphagia JE Richter, Ann Int Med, 1987
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Hypomotilty Disorders primary (idiopathic) aging produces gradual decrease in contraction strength reflux patients have varying degrees of hypomotility more common in patients with atypical reflux symptoms usually persists after reflux therapy defined as low contraction wave pressures (<30 mm Hg) incomplete peristalsis in 30% or > of wet swallows
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Hypomotilty Disorders secondary scleroderma in >75% of patients progressive, resulting in aperistalsis in smooth-muscle region incompetent LES with reflux other “connective tissue diseases” CREST polymyositis & dermatomyositis diabetes 60% with neuropathy have abnormal motility on testing (most asx) other hypothyroidism, alcoholism, amyloidosis
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Non ischemic Chest Pain remains poorly understood (functional chest pain) enthusiastic investigation finds numerous associations in studies psychiatric disorders (depression, panic or anxiety disorder…) esophageal disorders (GERD, motility disorders…) musculoskeletal disorders cardiac disease (microvascular, MVP, tachyarrhythmias…)
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Non ischemic Chest Pain GERD is by far the most common, diagnosable, esophageal cause 50-60% of patients have heartburn or acid regurgitation symptoms 50% have abnormal esophageal pH studies (not always correlating to sxs) very low incidence of endoscopic findings “PPI Test” may be best and most cost-effective approach a small subset of patients with non-GERD NCCP display a variety of esophageal motility disorders symptoms and motility findings correlate poorly esophageal hypersensitivity/hyperalgesia may explain the symptoms
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GERD 36-77% of all Americans experience GERD – 7% have daily GERD symptoms – 14-20% weekly symptoms – 15-50% monthly Symptoms include: heartburn, acid regurgitation, water brash, dysphagia, atypical symptoms (asthma, globus, laryngitis, cough, throat clearing)
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Pathophysiology Lower esophageal sphincter dysfunction Delayed gastric emptying Esophageal dysmotility +/- hiatal hernia Repetitive mucosal injury / esophagitis Barrett’s Esophagus
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Medical Treatment Lifestyle modifications – avoid coffee, fatty foods, smoking; lose weight, raise head of bed, eliminate late night meals Acid suppressin via PPI’s
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Indications for Surgery Failed medical management Need for lifelong medical therapy Hiatal hernia Atypical symptoms with (+) pH probe Complications – Barrett’s esophagus (5-15% develop BE) – Erosive esophagitis
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Surgical Treatment Pre-operative evaluation – Esophagram – EGD – Manometry (resting LES >5, length >2cm) – 24-hr esophageal pH monitoring
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Surgical Treatment Laparoscopic Nissen Fundoplication Goals of antireflux surgery: – Recreate Angle of His – Reconstitute LES with wrap Predictors of good surgical outcome: – typical symptoms (heartburn, regurg) – abnormal pH score, but NML motility – clinical response to acid suppression therapy
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Other New Treatments Stretta...radiofrequecy ablation of LES Enteryx, Gatekeeper...implanted biopolymer into LES Endocinch, Plicator...endoscopic suturing to recreate LES
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GERD Controversies Are meds better than antireflux surgery? Does antireflux surgery allow regression of Barrett’s esophageal better than meds? Which is more cost effective? Does symptom relief correlate with esophageal acid exposure? Where do the newer endoscopic therapies stand?
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Quiz? 51 yrs old lady presented with chest pain , difficulty to swallow, post prandial vomiting Endoscopy failed to intubate the esophagus PPI given Symptoms improve
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7/12/2021 LDLT 5th case 49 Thank You
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GERD Medical Vs Surgical Therapy In 1992, VA Cooperative study found open Nissen fundoplication better than antacids, H2 blockers in controlling GERD In 2001, VA Coop study follow-up at 10 years showed 62% of surgical arm used acid suppression meds for symptom control Few deaths due to esoph cancer, but study was underpowered to detect difference
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GERD Medical Vs Surgical Therapy A multicenter Nordic study evaluated treatment failures of Omeprazole to Nissen fundoplication – failure defined as: mod/severe heartburn, dysphagia or regurg; grade 2 esophagitis; > 8 wks post-op requiring PPI At 12 months surgery was favored But at five year follow-up, open surgery appeared superior, but when allowing for escalating doses of PPI, each strategy was similar for symptom control Lundell et al. Gastroenterology 114:A207, 1998. Lundell et al. JACS 192:172-179, 2001
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GERD Medical Vs Surgical Therapy UK study evaluated laparoscopic Nissen to PPI therapy in 217 randomized patients with chronic GERD At three months, LNF group had improved LES pressure, DeMeester acid eposure score, GI symptom and general well-being score as compared to PPI group, and lasted to twelve months Mahon et al. Brit Journ Surg 92:695-699, 2005.
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Regression Of Barrett’s PPI compared to LNF in 35 non-randomized pts with low-grade dyspasia detected on surveillance EGD 12 of 19 (63%) in PPI group had regression of LGD to Barrett’s compared to 15 of 16 (93%) of LNF pts at 12 and 18 months Is biliopacreatic reflux to blame for BE? Rossi et al. Annals of Surgery 243:58-63, 2006.
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DO Symptoms Correlate with Treatment (Success/Failure) 24 hr pH and DeMeester acid scores compared in 70 pts on no meds, on PPIs, or after antireflux surgery LES pH decreased most by LNF 18 of 30 PPI pts asymptomatic but had pathologic pH probe testing 19 LNF pts complained of heartburn/regurg, only two had positive pH probe Jenkinson et al. Brit Jour Surg 91:1460-1465, 2004.
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Hiatal Hernia
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Pathophysiology & Classification Type I - sliding Type II - paraesophageal Type III - para and sliding component Type IV - other viscera involved
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Clinical Presentation postprandial fullness (63%), Reflux (31%), Dysphagia (34%), Bleeding (24%) Regurgitation/vomiting (36%) Dyspnea (11%)
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Work Up
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Surgical Treatment Effective repair includes: – Excision of hernia sac – Reduction of hernia contents – Repair of crural defect – Fundoplication, gastropexy, PEG, esophageal lengthening (Collis gastroplasty)
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Upper Esophageal Motility Disorders
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Overview cause oropharyngeal dysphagia (transfer dysphagia) patients complain of difficulty swallowing tracheal aspiration may cause symptoms pharyngoesophageal neuromuscular disorders stroke Parkinson’s poliomyelitis ALS multiple sclerosis diabetes myasthenia gravis dermatomyositis and polymyositis upper esophageal sphincter (cricopharyngeal) dysfunction
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Overview cricopharyngeal hypertension elevated UES resting tone poorly understood (reflex due to acid reflux or distension) cricopharyngeal achalasia incomplete UES relaxation during swallow may be related to Zenker’s diverticula in some patients clinical manifestations localizes as upper (cervical) dysphagia within seconds of swallowing coughing, choking, immediate regurgitation, or nasal regurgitation diagnosis: swallow evaluation & modified barium swallow