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Esophageal Disorders PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Esophageal Disorders" by Dr. Salem M. Bazarah, MD, M.Ed, FACP, FRCPC, FRCPC(GI) & PhD.

This medical PowerPoint presentation is about esophageal disorders, medical conditions that affect the esophagus, the muscular tube that connects the throat to the stomach. Some common esophageal disorders include:

Gastroesophageal Reflux Disease (GERD): This condition occurs when stomach acid flows back into the esophagus, causing heartburn, chest pain, and other symptoms.
Esophageal Cancer: This is a malignant tumor that grows in the lining of the esophagus. It can cause difficulty swallowing, weight loss, and chest pain.
Achalasia: This is a rare disorder that affects the ability of the esophagus to move food down to the stomach. It can cause difficulty swallowing, chest pain, and regurgitation.
Esophageal Stricture: This is a narrowing of the esophagus that can cause difficulty swallowing and chest pain.
Barretts Esophagus: This is a condition in which the cells that line the esophagus are replaced by abnormal cells. It can increase the risk of developing esophageal cancer.
Esophagitis: This is inflammation of the lining of the esophagus. It can be caused by GERD, infections, or other factors.

Treatment for esophageal disorders varies depending on the specific condition and severity. It may involve medication, lifestyle changes, or surgical procedures. Its important to consult with a healthcare professional if you experience any symptoms related to your esophagus.

Tags : Esophageal Disorders, esophagus, Gastroesophageal Reflux Disease, Esophageal Cancer, Achalasia, Esophageal Stricture, Barretts Esophagus, Esophagitis, Otolaryngology, Otolaryngology PowerPoint presentation

Published on : Jun 23, 2023 | Views : 1340 | Downloads : 0

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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
Slide 2-

Esophageal Disorders Motility Anatomic & Structural Reflux Infectious Neoplastic Miscellaneous
Slide 3-

Esophageal Anatomy Upper EsophagealSphincter (UES) Lower EsophagealSphincter (LES) Esophageal Body(cervical & thoracic) 18 to 24 cm
Slide 4-

Normal Phases of Swallowing Voluntary oropharyngeal phase – bolus is voluntarily moved into the pharynx Involuntary UES relaxation peristalsis (aboral movement) LES relaxation
Slide 5-

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
Slide 6-

Normal Swallowing Cortical Swallowing Areas Swallowing Center Motor Nuclei Oropharynx & Esophagus Frontal cortex Brainstem
Slide 7-

Esophageal Motility Disorders
Slide 8-

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
Slide 9-

Diagnostic Tools cineradiology or videofluoroscopy (MBS) barium esophagram esophageal manometry endoscopy
Slide 10-

Normal Manometry
Slide 11-

Motility DisordersBased on Manometry Achalasia – Inadequate LES relaxation Diffuse Esophageal Spasm – Uncoordinated contraction Nutcracker Esophagus – Hypercontraction Ineffective Esophageal Motility – Hypocontraction
Slide 12-

Achalasia
Slide 13-

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
Slide 14-

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
Slide 15-

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
Slide 16-

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
Slide 17-

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)
Slide 18-

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Slide 19-

Manometric Features Incomplete LES relaxation Elevated resting pressure (>45 mmHg) Aperistalsis of esophageal body
Slide 20-

Treatment of Achalasia
Slide 21-

Goals reduce LES pressure and increase emptying
Slide 22-

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
Slide 23-

Botulinum Toxin prevents ACH release at NM junction 90% initial response; 60% at 1 year Needs repetitive sessions
Slide 24-

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%
Slide 25-

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
Slide 26-

Spastic Motility Disorders of the Esophagus
Slide 27-

Spastic Motility Disorders of the Esophagus Diffuse Esophageal Spasm Nutcracker Esophagus Hypertensive LES Nonspecific Esophageal Dysmotility
Slide 28-

Epidemiology Any age (mean 40 yrs) Female > Male
Slide 29-

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
Slide 30-

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”)
Slide 31-

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
Slide 32-

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
Slide 33-

Diagnosis of Spastic Motility Disorders of the Esophagus Manometry Barium Esophagram Endoscopy PH monitoring
Slide 34-

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
Slide 35-

Manometry in Esophageal Symptoms Non-Cardiac Chest Pain Dysphagia JE Richter, Ann Int Med, 1987
Slide 36-

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
Slide 37-

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
Slide 38-

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…)
Slide 39-

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
Slide 40-

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)
Slide 41-

Pathophysiology Lower esophageal sphincter dysfunction Delayed gastric emptying Esophageal dysmotility +/- hiatal hernia Repetitive mucosal injury / esophagitis Barrett’s Esophagus
Slide 42-

Medical Treatment Lifestyle modifications – avoid coffee, fatty foods, smoking; lose weight, raise head of bed, eliminate late night meals Acid suppressin via PPI’s
Slide 43-

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
Slide 44-

Surgical Treatment Pre-operative evaluation – Esophagram – EGD – Manometry (resting LES >5, length >2cm) – 24-hr esophageal pH monitoring
Slide 45-

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
Slide 46-

Other New Treatments Stretta...radiofrequecy ablation of LES Enteryx, Gatekeeper...implanted biopolymer into LES Endocinch, Plicator...endoscopic suturing to recreate LES
Slide 47-

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?
Slide 48-

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
Slide 49-

24-Jun-23 LDLT 5th case 49 Thank You
Slide 50-

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
Slide 51-

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
Slide 52-

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.
Slide 53-

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.
Slide 54-

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.
Slide 55-

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
Slide 57-

Clinical Presentation postprandial fullness (63%), Reflux (31%), Dysphagia (34%), Bleeding (24%) Regurgitation/vomiting (36%) Dyspnea (11%)
Slide 58-

Work Up
Slide 59-

Surgical Treatment Effective repair includes: – Excision of hernia sac – Reduction of hernia contents – Repair of crural defect – Fundoplication, gastropexy, PEG, esophageal lengthening (Collis gastroplasty)
Slide 60-

Upper Esophageal Motility Disorders
Slide 61-

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
Slide 62-

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, ornasal regurgitation diagnosis: swallow evaluation & modified barium swallow