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Esophageal Motility Disorders. Anatomy. Active muscular organ with a complex neuromuscular structure and integration. The sequential muscular contractions push food from above and clear acid and bile reflux from below. Specialized sphincter at each end. UES and LES. Anatomy.

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Esophageal Motility Disorders

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  • Active muscular organ with a complex neuromuscular structure and integration.
  • The sequential muscular contractions push food from above and clear acid and bile reflux from below.
  • Specialized sphincter at each end.
  • UES and LES
  • UES contracts during inspiration preventing air from entering into the GI tract, while the LES maintains a steady baseline tone to prevent gastric juice from refluxing into the esophagus.
  • LES also contracts during periods of increased intraabdominal pressure, preventing reflux due to pressure in the abdomen.
  • Inner circular layer, outer longitudinal layer of muscle. (ring occlusions and shortens)=> peristalsis.
  • Sequential, coordinated contraction wave that travels along the whole length of the esophagus, propelling intraluminal contents downstream.
  • Primary wave strips from proximal to distal, triggered by swallowing center, 2cm/sec.
  • Secondary wave induced by distension of bolus, acts to clear esophagus of retained food.
  • Tertiary contractions are dysfunctional and have no role.
motility disorders
Motility Disorders
  • Achalasia
  • Primary spastic motility disorders, including DES, nutcracker esophagus, hypertensive LES
  • Secondary esophageal motility disorders related to DM, scleroderma, alcohol, psychiatric disorders, etc.
  • Loss of ganglion cells from the wall of the esophagus, starting at the LES and going proximally.
  • Loss of inhibitory nerves at LES.
  • Circular muscle layer thickened at LES but microscopically cells appear normal.
  • Loss of the inhibitory nerves at the LES causes failure of the LES to completely relax, and a hypertensive LES pressure over 40mmHg in 60% of patients.
  • Loss of nerves along the body of esophagus causes aperistalsis, stasis, dilatation.
  • Non-peristaltic isolated contractions or low-amplitude simultaneous contractions occur.
  • If high-amplitude (>60mmHg) simult contractions occur it is called Vigorous Achalasia.
  • Edrophonium (acet cholesterase inhib) increases LES pressure.
  • Atropine reduces the LES pressure in achalasia, which is why botulinum toxin can be therapeutic (ach release inhibitor).
spastic motility disorders
Spastic Motility Disorders
  • Diffuse fragmentation of vagal filaments, mitochondrial fragmentation results in functional imbalance between excitatory and inhibitory pathways.
  • When DES occurs, diffuse muscular hypertrophy as much as 2cm has been described in the distal 2/3 of the esophagus, but wall thickening is also found in asymp patients, absent in patients with typical sympt and manometric findings too.
scleroderma esophagus
Scleroderma Esophagus
  • Primary defect here is related to smooth muscle atrophy and fibrosis.
  • The dysmotility here an absence of peristalsis in the esoph body and an atonic LES occur.
  • Motility is preserved at the striated muscle part of the esophagus.
  • Achalasia and DES only a small percentage of disorders of motility.
  • Achalasia 1 case per 100,000 per year.
  • Familial clustering occurs but not genetic yet.
  • Nutcracker esoph is most common motility disorder, but the most controversial in significance.
mortality and morbidity
Mortality and Morbidity
  • Achalasia associated with significant progressive discomfort, severe dysphagia, malnutrition, weight loss, dehydration. Increased incidence of SCC with long standing disease.
  • Spastic motility disorders are associated with sympt discomfort but not the severity of dysphagia as in achalasia.
  • Scleroderma associated with severe acid reflux, associated complications, including strictures, Barretts, adenocarcinoma.
race sex and age
Race, Sex, and Age
  • Racial differences not established.
  • Affects both sexes equally.
  • Achalasia presents in patients 25-60 yrs, although it can affect any age group.
  • Achalasia: progressive dysphagia for both solids an liquids is a hallmark. Regurge of food in dilated esoph common especially at night. Chest pain, sensation of heartburn (fermentation). Emotional stress or rapid eating makes it worse.
  • Spastic disorders: Chest pain hallmark, mimics angina, may be related to transient esoph ischemia, distension. Dysphagia to solids and liquids a common symptom, especially with DES, intermittent, non-progressive. Heartburn, regurge.
  • Scleroderma: involves esoph in 75% of patients.
  • Two forms- PSS a progressive form that is more fulminant, early involvement with internal organs; CREST- calcinosis, Raynauds phenomena, esoph dysfunction, sclerodactyly, telangiectasia.
  • Severe acid reflux, regurge, dysphagia, erosive esophagitis (60%), increased incidence of cancer
  • Dysphagia from peptic strictures, poor peristalsis.
  • Results of a physical exam are usually unrevealing.
  • Pay attention to signs of scleroderma in proper clinical setting.
  • A bedside swallowing challenge can be performed with a glass of water.
  • Check nutrition and hydration if dysphagia reported.
  • Primary disorders are idiopathic in nature.
  • Viral
  • Infectious
  • Environmental
  • Genetic
other problems
Other Problems
  • Differential diagnosis depends on presenting symptoms.
  • CAD, mechanical obstructing lesions, benign or malignant should be ruled out.
  • Differential of achalasia includes Chagas disease secondary to Trypanosoma cruzi infection and pseudoachalasia from GE junction tumors.
chagas disease
Chagas Disease
  • Mimics achalasia.
  • Reduviid (kissing) bug bite.
  • Endemic in SA, CA.
  • Septicemia first, then chronic stage ensues.
  • Widespread ganglion destruction throughout the body involving heart, gut, GI tract, urinary tract, respiratory tract.
  • Symptoms take years to develop.
  • Treatment: disrupt LES like in achalasia.
  • Term used to describe clinical picture of GE junction obstruction.
  • Present in 5% of patients with clinical and manometric diagnosis of achalasia.
  • Clinical presentation is more likely to occur with rapidly progressive disease, older age of onset, profound weight loss.
  • Workup includes upper endoscopy, biopsies should be obtained with any suspicion of malignant process. If suspicious lesion found, image with CT, MRI, EUS if indicated.
  • In 50% of patients the diagnosis is adenocarcinoma of GE junction.
diffuse esophageal spasm1
Diffuse Esophageal Spasm
  • DES and achalasia can be confused. Manometric criteria require that normal esophageal peristalsis be present intermittently for DES.
  • LES relaxation, which is incomplete in achalasia, should be normal in DES.
  • CXR: Dilated esophagus, looks sigmoid like, air fliud level, wide mediastinum, absence of gastric air bubble.
  • Esophagram: In achalasia, dilated, A-F level, tapered LES, bird’s beak appearance. Diverticula above LES, hiatal hernia. In DES corkscrew or rosary bead esophagus. In scleroderma, slightly dilated esophagus, absent peristalsis, free reflux.
  • Achalasia: aperistalsis of esophageal body is manometric hallmark.
  • DES: Normal peristalsis, simultaneous contractions in >30% water swallows, incomplete LES relaxation, increased LES pressure (>40mmHg), or repetitive, prolonged(>6sec), high-amplitude contractions (>180mmHg).
  • Nutcracker: Normal patterned peristalsis with high amplitude contractions(>180mmHg), repetitive contractions, increased LES pressure(>40mmHg).
  • Hypertensive LES: Increased LES pressure (>40mmHg). Significance of this is questionable.
  • Exclude mechanical and inflammatory lesions that are causing dysmotility, structural cause of obstruction.
  • Endoscopic US still investigational in managing achalasia, used to assist in botulinum toxin injection.
pharmacological treatment
Pharmacological Treatment
  • Smooth muscle relaxants including Ca channel blockers, nitrates. Also used, anticholinergics, amyl nitrite, NTG, theophylline, ,beta-2-agonists. Experience with these are limited in comparison to the first two.
pharmacological treatment1
Pharmacological Treatment
  • Spastic Disorders: antireflux therapy, TCA, trazodone.
  • Botulinum toxin injection: into the LES used to treat pts with achalasia. A potent inhibitor of ach release from nerve terminals. May be a good alternative for poor surgical candidates, disadvantage is high cost and need for repeated injections.
endoscopic therapy
Endoscopic Therapy
  • EGD with pneumatic dilatation is the standard for achalasia. Forceful distension of the LES to 3cm with disruption of the circular muscle layer is needed for symptomatic relief.
  • Complication is perforation (8%)
  • If pressure after is less than 10mmHg, outcome excellent.
surgical care
Surgical Care
  • Surgical treatments target the LES to relieve the high pressure.
  • Heller myotomy is procedure of choice for achalasia. It decreases the LES pressure across GE junction and eliminates dysphagia.
  • Myotomy may lead to GE reflux, so a fundoplication may be necessary with the myotomy.
surgical care1
Surgical Care
  • Heller myotomy is performed thru either transthoracic or transabdominal approaches.
  • Efficacy is 60-100% in different series.
surgical care2
Surgical Care
  • Esophagectomy with gastric pull up or intestinal interposition for patients with advanced disease or refractory cases, unresolved symptoms, carcinoma, perforation during dilation.
  • Extended Heller Myotomy last resort for DES when pain or dysphagia is severe.
  • Operation is a myotomy that starts at the LES and goes to thoracic inlet.