Lecture 17Esophageal diseases

Date of lecture: 11-11-209

Date of delivery: 12-11-2009
Done by: Suleiman Ghunaim

Good afternoon fellow doctors, its going to be a pretty easy lecture. I have added some
extra notes from Kumar and Clark Clinical Medicine book but you wont tell the
difference =)
Lets start by remembering the anatomy, physiology and histology of the esophagus..
The esophagus is a 20-30 cm long hollow tube connecting the pharynx to the stomach.
It passes through the posterior mediastinum posterior to the trachea and traverses the
diaphragm at its hiatus.
It is divided into the upper and lower esophagus.
Upper 1/3
Striated Skeletal outer longitudinal and
inner circular muscles.
Separated from the pharynx by the UES
which is made up from the fibers of the
cricopharyngeus muscle. The UES is
always closed due to the tonic activity of
its innervations and opens only the
moment we swallow.

Lower 2/3
Outer longitudinal and inner circular
smooth muscles.
Forms the gastro-esophageal junction (Zline) at the level of the LES which has a
high resting tone (20mmHg) that plays an
important role in preventing reflux. The
LES is always closed due to the tonic
activity of its innervating vagus nerve and
opens only the moment we swallow.

Histology:
- Made up of stratified squamous epithelium rich in glycogen that appears light in colour
on endoscopy.
- An underlying lamina propria with an underlying thin layer of smooth muscularis
mucosa.
- The outer muscular layer.
- No serosal covering This point is very important because any esophageal malignancy
spreads and metastasizes rapidly outside the esophagus, so whenever we diagnose an
esophageal cancer we must take into consideration the fact that it might have already
metastasized.
The esophagus is not just a hollow tube; it is a functioning organ with continuous
peristaltic wave activity. A peristaltic movement occurs every < 7 sec with an amplitude
of <150mmHg.

Esophageal diseases
Esophageal diseases are divided into:
1- Motor Disorders
a) Achalasia (discussed later)
b) Localized esophageal spasm

Sustained uncoordinated high

amplitude peristaltic contractions
associated with chest pain similar to
that of ischemic heart disease.

c) Diffuse esophageal spasm

d) Nutcracker esophagus..Very high amplitude peristaltic contractions up to 240mmHg

2- Organic (Structural) Disorders

Achalasia
It is defined as esophageal aperistalsis and impaired relaxation of LES. LES will stay
closed and will not open normally when we swallow unless there is a huge mass of bolus
with gravity forcing a small amount of food to pass.
Causes of Achalasia:
The exact etiology is unknown, but may be autoimmune, neurodegenerative or viral.
Histopathology shows inflammation of the mesenteric plexus of the esophagus with
possible: 1- Reduction in intramural ganglion cell numbers.
2- Loss of inhibitory nitrergic neurons.
3- Degenerative lesions in the vagus nerve.
Clinical Features:
The disease can be present at any age but rarely in childhood equally in males and
females.
1- Intermittent, long standing (years) Dysphagia for both liquids and solids (motor
disorder)
2- Regurgitation of food particularly at night
3- Chest pain (may be misdiagnosed as ischemic heart pain)
4- Aspiration recurrent pneumonia
5- Halitosis (stagnation of food + body temperature = !) .. =)
6- Weight loss

Investigations:
1-Manometry: is the best method for diagnosis of achalasia. Manometry is used to assess
the motility and contractions of the esophagus; this is done by inserting a probe through
the nose into the esophagus and measuring the pressure generated within the LES region.
Typical findings include:
1- Absent peristalsis
2- Increased LES pressure
3- Failure of LES relaxation

Notice how peristaltic waves in normal esophagus are

moving in sequence, contraction after contraction while in
achalasia there is reduced peristaltic movement and very
low wave irregular contractions. Notice the elevated LES
pressure with poor sphincter relaxation compared to
normal.

2- Radiologically by barium swallow, not the best method of diagnosis

Food stagnation
and esophageal
dilatation

Impaired
relaxation of
LES.

NORMAL =)

Rat tail image of

Achalasia =(

3- Endoscopy is done to exclude any malignancy, strictures or any organic abnormality

and is not diagnostic for achalasia.

Treatment:
1- Balloon dilatation is the most effective treatment- inserted through endoscope it
might be effective for one year only then symptoms reappear.
2- Medical treatment using smooth muscle relaxants (not very effective)
3- Surgical Myotomy is done laproscopically.
Reflux esophagitis complicates all procedures and the aperistalsis of the esophagus
remains!

Before we talk about Gastro-esophageal reflux disease here are some definitions:

Gasrtoesophageal reflux: Reflux of gastric contents to the esophagus which is

normal and is not called a disease unless it involves a change in the persons
lifestyle or ..

Gastroesophageal reflux disease (GERD): Any significant symptomatic clinical

condition (heartburn or regurgitation) more than twice a week or
histopathological changes resulting from reflux.

Reflux esophagitis: GERD patients with histopathologically demonstrable

changes in the esophageal mucosa.

Erosive reflux esophagitis (ERD) when endoscopic erosions are present

Non-erosive reflux esophagitis (NERD) when symptoms of reflux present with

normal endoscopy.

Gastro-Esophageal reflux disease

Epidemiology:
It is a very very common disease, 25% of all people at least suffer from it monthly.
More common in : 1- Pregnancy.. 80%
2- Obesity
3- Alcohol consumption and cigarette smoking
4- Large meals
Etiology:
1- Transient LES relaxation, the most common cause. Relaxation of LES is now
unrelated to swallowing, it can relax at any time. Notice how it is different from
achalasia, achalasia patients never suffer from reflux disease or symptoms.
2- Hypotensive LES, a possible cause of transient LES relaxation
3- Decreased acid clearance
4- Hiatus Hernia (HH) herniation of the stomach through the diaphragmatic hiatus,
LES is now in the thoracic cavity surrounded by ve pressure,-
leads to
transient relaxation of LES.
5- Impaired Salivation. These patients suffer from inappropriate saliva secretion,
and since saliva is alkaline, it is needed to neutralize stomach acidity (the primary
causer of symptoms)

Clinical Picture: 1- Esophageal symptoms

2- Extra- Esophageal symptoms

Esophageal Symptoms:

HEARTBURN
Pathognomic for GERD
ACID REGURGITATION
Dysphagia (mainly for solids due to spasm in the inflamed area)
Chest pain (may mimic pain of ischemic heart disease) aggravated by bending,
drinking hot liquids and alcohol.
Water brash
Nausea and vomiting
Belching
Hiccough

Extra-Esophageal Symptoms:

Chronic cough
Asthma due to aspiration into the lungs
recurrent pneumonitis due to aspiration
nocturnal choking ( acid reflux
spasm in the bronchi) may mimic PND
hoarseness of voice
Posterior laryngitis with ulceration and granuloma formation.
sore throat
dental disease
Earache
Globus sensation

Investigations:
1- Endoscopy is performed to check for esophagitis and assess the degree of damage
in the esophageal mucosa.. Remember NERD patients have normal esophageal
appearance on endoscopy
2- The clinical picture ( regurgitation + heartburn)
3- 24- hour Ph monitor is performed in NERD patients and patients complaining of
bronchial asthma or chest pain with no obvious reason (difficult cases).., a probe
is inserted through the nose all the way to the stomach, stays for 24 hours and
then taken out. (is considered the best method for diagnosis)
4- MII (Multi-channel intra luminal impedance).. This test is performed on patients
suffering from non- acidic reflux
reflux of food contents, bile, and pancreatic
juice (dudeno-gastro-esophegeal reflux), it is similar to the 24- hour monitor in
structure, but has no significance in acidic or Ph measure since the reflux is not
acidic.
5- Barium swallow, not very specific may show an ulcerated lower esophagus and
demonstrate a hiatus hernia if present
6- Bernstein test Insert a catheter, pour some acid observe similar symptoms of
reflux disease.

Normal esophageal
mucosa, it is smooth
with no foldings.

linear + longitudenal
erosions, red and swollen
seen in esophagitis

Severe esophagitis, multiple

erosions all over the
circumference of the esophagus
with ulceration.

Complications:
1- Stricture formation and fibrosis due to healing of inflammatory and ulcered
lesions which in turn might lead to narrowing of the lower esophagus

dysphagia (mainly solids)
2- Chronic bleeding, if ulcerations were deep
3- Affects the quality of life
4- Barretts disease and tissue metaplasia

Barretts

Barretts esophagitis is characterized by the transformation of the

normal esophageal squamous epithelium to gastric columnar
epithelium due to continuous acidic irritation from gastric reflux.
Barretts disease occurs in about 2% of all people suffering from
GERD and is associated with increased risk of adenocarcinoma.
Statistics show that it is pretty rare do develop this type of cancer
(about 0.5%)

Adenocarcinoma

History and Presentation:

GERD is mostly recurrent and chronic, the patient usually complains of symptoms over
long periods of time. It is rarely acute.
The majority of GERD patients respond well to treatment and may need some sort of acid
suppression therapy.
There is no clear relation between: a) the degree of inflammation and the amount of
reflux
b) the amount of reflux and the symptoms

Treatment:

Life- style modification:

avoid cigarette smoking
dietary manipulation: decrease fatty, spicy and acidic foods
decrease weight
elevation of the head of the bed
avoid tight abdominal binders( pressure on the stomach)
avoid large meals
avoid drugs which decrease LES pressure(anticholinergics)

avoid sleeping after meals for at least 3 hours.

Pharmacological Treatment:

Here the doctor didnt explain much, most of there drugs are explained more in the next
lecture.
1)
-Anti-acids : Al,Ca,Na,Mg compounds
-H2 blockers: famotidine, ranitidine, nasitidine.
-PPI (proton pump inhibitors): prazole compounds (omperazole, lansoprazole..)
2)
Prokinetic agents can be used to stimulate the LES to contract since it transiently
relaxes such as : domperidone, metclopramide.
3)
Endoscopic procedures (the doctor didnt explain at all) such as Serrata,Entyrex,.
4)
Surgery (laparoscopic fundiplication) is done to narrow the LES, it is done in
complicated cases, upon patients request or in patients that are not responding to the
normal antiacid therapy. LES relaxation may recur after 10 years.
5)
Finally, treatment of Barretts esophagus is only done by drugs and no surgery is
performed esophagetomy is done if there was severe metaplasia
Ablation of Barretts can be also performed ( ):

Photodynamic therapy: PDT

Argon plasma coagulation: APC
Endoscopic mucosal resection: EMR

A7la Ta7iyyeh la EMAD ZIBDEH w MOHAMMAD KURD!! =D

thank you so much for helping me throughout this lecture
Ta7iyyat min IRBID 2ila LONDON
Ta7iyye lal final destination (4D)
Special thanks to 3ala2, Walid, Jad, 3bedat, Oday Khammash..
Special thanks to my group (A5)
Ta7iyye la sport boy and his toys
Ta7iyye lal Congress w l menu
Ta7iyye lal Mulazem
Ta7iyye la Princess Basma Hospital w il H1N1
Ta7iyye lal Mutrab w YALLLLAAAAA>..
Ta7iyye la JD..
All the best to the rest of my collegues..
By: Suleiman Ghunaim