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Esophageal Motility Disorders

The document discusses various motility disorders of the esophagus including achalasia, diffuse esophageal spasm, nutcracker esophagus, and GERD. It covers the anatomy, mechanism of swallowing, classification, clinical presentation, diagnosis, and management of these disorders.

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0% found this document useful (0 votes)
74 views61 pages

Esophageal Motility Disorders

The document discusses various motility disorders of the esophagus including achalasia, diffuse esophageal spasm, nutcracker esophagus, and GERD. It covers the anatomy, mechanism of swallowing, classification, clinical presentation, diagnosis, and management of these disorders.

Uploaded by

georvin marco
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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Esophageal Motility

Disorders
PRESENTER : Dr Kwatwana,Dr.Hassan, Dr.Georvin
SUPERVISOR: Dr WAPALILA & Dr MOSE
OUTLINE
• INTRODUCTION
• ANATOMY
• MECHANISM OF SWALLOWING
• MOTILITY DISORDERS
ACHALASIA
DIFFUSE ESOPHAGEAL SPASM
NUTCRACKER
GERD
OBJECTIVES
• To describe anatomy of the Esophagus
• To understand the classification of motility disorders
• To learn about clinical presentation of motility disorders
• To describe the diagnosis of motility disorders
• To understand management of motility disorders
INTRODUCTION
• Normal swallowing requires the coordinated activity
of the oral cavity, pharynx, and esophagus.
• A properly functioning swallowing mechanism
provides efficient, unidirectional flow of the ingested
bolus, while avoiding undesired diversion into the
nasal cavity or respiratory tree.
ESOPHAGEAL ANATOMY
It is a hollow muscular tube conduit between
pharynx and stomach
3 anatomical segments (Cervical , thoracic,
abdominal)
3 functional parts
 (UES-3cm muscular-Killian &Laimer’s triangles ,
Body, LES-3cm muscular-)
Blood supply
Innervation
Mechanism of swallowing
A gullet is a mechanical model
Tongue and pharynx function like piston pump with three
valves
The three valves in the pharyngeal cylinder are the soft
palate, epiglottis, and cricopharyngeus.
The body of the esophagus and cardia function as a worm-
drive pump with a single valve , the LES.
Regulation of swallowing
The afferent sensory nerves of the pharynx are the
glossopharyngeal nerves and the superior laryngeal branches
of the vagus nerves.
Once aroused by stimuli entering via these nerves
 the swallowing center in the medulla coordinates the
complete act of swallowing by discharging impulses through
cranial nerves V, VII, X, XI, and XII, as well as the motor
neurons of C1 to C3.
CLASSIFICATION OF EMD
• primary
upper esophageal
disorders
• achalasia
UES disorders
• diffuse
neuromuscular
esophageal
disorders
spasm
• nutcracker
• esophageal esophagus
body
•• nonspecific
achalasia esophageal dysmotility
• secondary
• diffuse disorders
esophageal spasm
• severe esophagitis
nutcracker esophagus
• nonspecific esophageal dysmotility
scleroderma
• LES• diabetes
•• Parkinson’s
achalasia
•• stroke
hypertensive LES
ACHALASIA
• Achalasia is primary a disorder of motility of the lower
oesophageal or cardiac sphincter.
• The smooth muscle layer of the oesophagus has impaired
peristalsis and failure of the sphincter to relax causes a
functional stenosis or functional oesophageal stricture.
EPIDEMIOLOGY
• The most common form is primary achalasia which is due to the
failure of distal esophageal inhibitory neurons.
• A small proportion occurs secondary to other conditions, such as
esophageal cancer or Chagas disease (an infectious disease common in
South America).
• Achalasia affects about one person in 100,000 per year.
• Prevalence of the condition is 10 in 1,000,000 individuals.
• There is no gender predominance for the occurrence of disease
PATHOGENESIS

•LES pressure and relaxation are regulated by excitatory (e.g., acetylcholine,


substance P) and inhibitory (e.g., nitric oxide, vasoactive intestinal peptide)
neurotransmitters.
•Loss of ganglion cells within the myenteric (Auerbach's) plexus
•Persons with achalasia lack non-adrenergic, non-cholinergic, inhibitory ganglion
cells, causing an imbalance in excitatory and inhibitory neurotransmission.
•The result is a hypertensive non-relaxed esophageal sphincter.
• Hypertrophy and degeneration of oesophageal muscle
CLINICAL PRESENTATION
• Dysphagia

• Regurgitation (80-90%)

• Chest Pain (17-63%)

• Heartburn/Cough/Recurrent Chest Infection/Weight loss


DIAGNOSIS
Barium Swallow- A peristalsis of distal esophagus, bird beaking,
dilation of the esophagus

Endoscopy and Biopsy-excess stale of food in the esophagus,


candidiasis

Manometry-absence of peristalsis, pressure maybe hypertonic or


hypotonic and non relaxing sphincter(distal barrier function).
Figure 1 Esophagograms of a patient with achalasia .

GI Motility online (May 2006) | doi:10.1038/gimo53


High-Resolution Manometry (HRM)
This “high-resolution manometry” is a variant of the conventional
manometry in which multiple, circumferential recording sites are
used, in essence creating a “map” of the esophagus and its
sphincters.
High-resolution catheters contain 36 miniaturized pressure sensors
positioned every centimeter along the length of the catheter. High-
resolution manometry may allow the identification of focal motor
abnormalities previously overlooked.
It has enhanced the ability to predict bolus propagation and
increased sensitivity in the measurement of pressure gradients
Esophageal Transit Scintigraphy.
• The esophageal transit of a 10-mL water bolus containing technetium-
99m (99mTc) sulfur colloid can be recorded with a gamma camera.
• Using this technique, delayed bolus transit has been shown in
patients with a variety of esophageal motor disorders, including
achalasia, scleroderma, DES, and nutcracker esophagus.
Video- and Cineradiography
• High-speed cinematic or video recording of radiographic studies
allows re-evaluation by reviewing the studies at various speeds.
• This technique is more useful than manometry in the evaluation of
the pharyngeal phase of swallowing.
Medical Treatment

•Drugs that reduce LES pressure are useful.


•Calcium channel blockers such as nifedipine
• Nitrates such as isosorbide dinitrate and nitroglycerin.
• However, many patients experience unpleasant side effects such as
headache and swollen feet, and these drugs often stop helping after
several months.
• Botulinum toxin (Botox) may be injected into the lower esophageal
sphincter to paralyze the muscles holding it shut.
Pneumatic dilatation

In balloon (pneumatic) dilation or dilatation, the muscle fibers are


stretched and slightly torn by forceful inflation of a balloon placed
inside the lower esophageal sphincter.
There is always a small risk of a perforation which requires immediate
surgical repair, scarring which may increase difficulty in Heller's
myotomy and GERD in some patients.
 Pneumatic dilatation is most effective on the long term in patients
over the age of 40; the benefits tend to be shorter-lived in younger
patients
SURGICAL TREATMENT
Heller myotomy helps 90% of achalasia patients.
It can usually be performed by a keyhole approach, or
laparoscopically.
The myotomy consists of longitudinal division of the muscle fibres of
the lower esophagus, and should extend across the oesophagogastric
junction for 1–2 cm to ensure the division of all constricting muscle
fibres.
Traditionally, an extensive myotomy was performed through a left
posterolateral thoracotomy.
Preoperative management prior to a Heller’s cardiomyotomy
includes the insertion of a wide-bore nasogastric tube, but removal of
solid food retained in the dilated esophagus is still difficult.
The anesthetist should be aware of the aspiration risk during
induction and should protect the airway appropriately.
Broad-spectrum antibiotic prophylaxis is usually recommended on
induction.
Heller Cardiomyotomy
Fundoplication After Myotomy
DIFFUSE ESOPHAGEAL SPASM(DES)
 DES is defined as a clinical entity associated with abnormal
esophageal contractions .
Although the etiology is unclear, it likely represents a selective, often
intermittent, dysfunction of the myenteric plexus.
CLINICAL PRESENTATION
Diffuse esophageal spasm is characterized clinically by intermittent
chest pain and dysphagia( solids or liquids esp very hot or cold foods).
Chest pain can vary from mild to crushing, extend to the back and
jaw, and last from seconds to minutes.
 The pain with DES does not always occur with swallowing.
Regurgitation is infrequent.
The symptoms of DES can range from mild to severe classically
intermittent.
DES is defined by manometric criteria rather than by clinical,
functional, or pathologic criteria.
It also differs from achalasia in that it is usually an intermittent
phenomenon, with the esophagus alternatively exhibiting normal
primary peristalsis.
‘Corkscrew esophagus’ in diffuse esophageal spasm
NUTCRACKER ESOPHAGUS
Nutcracker esophagus, which also classically presents with chest pain
and dysphagia, is characterized manometrically by a mean distal
esophageal peristaltic amplitude of more than 180 mm Hg.
Minor criteria for NE include repetitive contractions (>2 peaks) that
are prolonged (>6 seconds).
ENDOSCOPY
• Endoscopic Findings
The esophagus is usually normal in appearance in patients with DES
and NE, but a thorough search for signs of GERD (esophagitis,
ulcerations, stricture, etc) should be performed at the time of upper
endoscopy.
Pharmacology.
Muscle relaxants such as nitrates, calcium channel antagonists, and
even botulinum toxin have been used to treat DES and NE, with
various results.
Antireflux agents (predominantly histamine receptor antagonists and
proton pump inhibitors).
Endoscopic dilatation. E.g. bougienage and pneumatic balloon.
SURGERY

The traditional surgical approach to spastic disorders of the


esophagus has been esophageal myotomy.
Myotomy performed either laparoscopically or thoracoscopically is
primarily reserved for patients with DES or NE in whom medical
therapy has failed.
GERD
Gastro esophageal reflux disease (GERD) is a condition in which
reflux of gastric contents into the esophagus produces frequent or
severe symptoms that negatively affect the individual’s quality of life
or result in damage to esophagus, pharynx, or the respiratory tract.
PATHOPHISIOLOGY OF GERD

• The pathophysiology of GERD is complex.


• Normally small amount of gastric contents reflux through cardia, most
common after meal associated with belching
• Refluxed materials triggers secondary peristalsis which clear the
esophagus
• Esophagitis develops when these mechanisms are impaired
• Usually is limited to 7-10cm,primarily caused by acid and pepsin: bile
acid s in patients had gastric surgery.
GERD most often occurs when LES pressure is low or the normal
angulation of the EG junction is lost (as occurs when a hiatus hernia is
present) and due to increased intrabdominal pressure
Usually occur at night: transient relaxation of LES, refluxed material
is acid and pepsin no food, decreased esophageal peristalsis (delaying
clearance), less saliva
Inflammation-low secondary peristalsis-further exposure to acid-
damage-complications
DIAGNOSIS
Esophagoscopy
• To note mucosal changes
Esophageal biopsies
• To note changes at the cellular level
Motility studies
• Low LES pressures are associated with reflux
pH monitoring
• The most precise measure for the presence of acid in the esophageal lumen
(24 hour monitoring)
Endoscopic Evaluation.
When GERD is the suspected diagnosis
Detection of the presence of esophagitis and Barrett’s columnar-lined
esophagus (CLE) is very significant.
ESOPHAGEAL MANOMETRY
In patients with symptomatic GERD, manometry of the esophageal
body can identify a mechanically defective LES, and evaluate the
adequacy of esophageal peristalsis and contraction amplitude.
The pressure, abdominal length, and overall length of the sphincter
are determined.
TREATMENT:
Treatment of reflux disease can be divided between
medical and surgical approaches.
The vast majority of patients can be treated
effectively by a combination of life-style modifications
and drug therapy.
Surgery is indicated in medical therapy failure or
complication
1.LIFESTYLE:
• Avoid caffeinated beverages- increase gastric acidity.
• Avoid fatty foods, chocolates- decrease LES pressure,
gastric emptying
• Avoid coffee, alcohol and acidic liquids- affect esophageal
peristalsis.
• Avoid large meals
• Avoid smoking-affects esophageal motor fxn, air
swallowing
• Avoid lying down after meals.
• Elevate the head of the bed.
• Reduce weight (if overweight).
Drug Therapy
1.Acid suppressing agents
• Decrease gastric acidity
• Antacids
• H2 blockers
• PPI
2.Prokinetic agents
• Enhance UGI motility
• Effective as H2 blockers
• Used in combination
SURGERY:
Indications:
• Persistent complications GERD eg stricture
• Barrett's esophagus
• Respiratory complications eg Recurrent pneumonia,
asthma, laryngitis
• Persistent regurgitation
• Young patients,<40yrs
• Failure to respond to medical treatment
• Patients choice
Choice of Surgery:
• A number of surgical approaches have been
advocated.
• All involve an attempt to restore the GEJ and lower
5cm to the normal intrabdominal position,
approximating the crura to bolster the strength of the
antireflux barrier.
In general the several different types of antireflux
procedures can be classified as:
(1) Total fundoplication: Nissen and Rosetti-Hill.
(2) Partial fundoplication: Toupet and Watson
(3) Collis Procedure for Short Esophagus
The most commonly employed surgical approach is
referred to as a Nissen fundoplication .
 It involves a complete wrap (360 degrees) of the
lower 3-4 cm. sutured into place, relatively loose,
with a 56F dilator in the esophagus and buttressed to
the sides to prevent slipping
Nissen Fundoplication
• The essential elements necessary for the performance of a trans
abdominal fundoplication are
1. Hiatal dissection and preservation of both vagi along their
entire length
2. Circumferential esophageal mobilization
3. Hiatal closure, usually posterior to the esophagus
4. Creation of a short and floppy fundoplication over an esophageal
dilator
Technique of Nissen fundoplication; B’, endoscopic view
Hill Fundoplication)
PARTIAL FUNDOPLICATION
Partial fundoplication were developed as an alternative to the Nissen
procedure in an attempt to minimize the risk of post fundoplication
side effects, such as dysphagia, inability to belch, and flatulence.
a partial fundoplication is constructed in patients with impaired
esophageal motility, in which the propulsive force of the esophagus is
thought to be insufficient to overcome the outflow obstruction of a
complete fundoplication.
COMPLICATIONS OF FUNDOPLICATION
Recurrence of reflux symptoms
Dysphagia
Wrap migration
Post vagotomy syndrome- gastro-paresis, diarrhea
Post bloat syndrome
ENDOSCOPIC TECHNIQUES IN TREATMENT OF GERD
Suturing, EndoCinch (Bard)
• Full-thickness Plication (NDO Surgical)
• Flexible Sewing device (Wilson Cook)
Radiofrequency Energy (Stretta System)
Injection/Implant
• Enteryx (Boston Scientific)
• Gatekeeper Hydrogel Prosthesis (Medtronic)
INDICATIONS FOR ENDOSCOPIC TREATMENT OF GERD
Non-Surgical candidates who suffer from the
following conditions:
Poor or absent peristalsis with bad reflux
Elderly patients who fail medical therapy
Volume refluxer
• References
• Subiston textbook of chest surgery
• Schwartz Principles Of Surgery 11 edition
• The mont Reid surgical hand book
• Atlas of human anatomy by Frank H. Netter
• Current surgical diagnosis and Treatment 11th edition

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