ESOPHAGEAL PATHOLOGY

General notions

o Esophagus - organ tubulo-membranous; L = 20 cm, diameter = 1-3 cm

o It connects the pharynx to the stomach; extends from the lower edge of the cricoid cartilage
(corresponding to the C6 vertebra) to the level of the T11 vertebra
o It has 3 sections:
§ Esophagus in the cervical region - crosses the middle of the neck, slightly deviated to the left,
positioned posteriorly by the trachea and anteriorly by the spine.
§ The esophagus in the thoracic region - is positioned in a posterior plane of the trachea, behind
the large vessels.
§ Esophagus in the abdominal region - enters through the esophageal hiatus of the diaphragm.
The esophagus connects to the stomach through cardia; at this level is the lower esophageal
sphincter.

— At the cervical esophagus - there are striated muscle fibers arranged in two layers - internal circular and
external longitudinal
— In the lower two thirds of the esophagus (thoracic and abdominal), also containing the lower esophageal
sphincter - the muscle wall consists of two smooth muscle layers
— The esophageal mucosa - covered with stratified squamous epithelium -> extends distally to the
squamous-cylindrical junction between the esophagus and the stomach, with a zigzag appearance, called
the "z" line, located just above the first proximal gastric folds
— Upper esophageal sphincter (UES) - separates the pharynx from the esophagus; it is closed between
swallowing due to the tonic activity transmitted by the nerve threads that innervate the cricopharyngeal
muscle
— Lower esophageal sphincter (LES) - area of 2-4 cm at the distal end of the esophagus; has an increased
resting pressure which, together with the diaphragmatic sphincter, prevents the reflux of gastric contents
into the esophagus

GASTRO-ESOPHAGEAL REFLUX DISEASE (GERD)

— All symptoms caused by reflux of gastric contents into the esophagus, with / without lesions of the
esophageal mucosa
— 2 entities:
Ø negative endoscopic GERD - cases that meet the clinical definition but do not involve
endoscopic lesions
Ø positive endoscopic GERD - reflux esophagitis
— Prevalence of 10-20% in civilized countries
— More common in the Western world than in Asia

— Risk factors associated with GERD:

— Pregnancy and obesity — Achalasia treatment
— smoking — Antimuscarinic agents, calcium
— high fat diet, chocolate channel blockers, nitrates
— Coffee, alcohol — Scleroderma
— Hiatal hernia
Pathogeny
• Main cause - reflux of gastric acid, pepsin, bile and duodenal contents in the esophagus
• In GERD there is an incompetence of the natural mechanisms of protection against reflux:
Ø between swallowing, the muscles of the esophagus relax, except for the two sphincters; SEI
remains contracted due to its special muscular properties and relaxes at the onset of swallowing;
Transient relaxation of SEI is considered physiological, but is more common in GERD
Ø high abdominal pressure (ex. during pregnancy) and low SEI pressure predispose to GERD
Ø the intra-abdominal segment of the esophagus acts as a valve; the absence/shortening of this
segment determines the appearance of a pressure gradient that favors GERD
Ø His enlarged angle loses its ability to act as a flap that opposes the reflux of gastric

• Secondary peristalsis, gravity, and salivary bicarbonate neutralizes the acid reflux from the esophagus;
at night, salivary secretion ceases and the chemical clearance is delayed.
• The role of acid pocket in GERD - area in the proximal part of the stomach in which unstamped gastric
acid accumulates postprandially; it serves as a reservoir for acid reflux, especially in patients with hiatal
hernia, where the distal esophagus is located supradiaphragmatically, especially when the patient is in
clinostatism.

Symptomatology

Typical symptoms
Ø Heartburn
Ø Regurgitation
Ø Belching, sialorrhea, odynophagia
Ø Dysphagia
Atypical symptoms
ü nausea, vomiting, indigestion, early satiety, epigastric pain, bloating
ü asthma, wheezing, chronic cough, fibrosis, lung abscess
ü heartburn, gingivitis, erosions, dysphonia, foreign body sensation, laryngitis
ü sleep disturbances, nightmares, chest pain

Symptoms due to complications

ü dysphagia
ü retrosternal chest pain
ü hemorrhage
ü cough
ü hemoptysis

— Heartburn - the main symptom; painful retrosternalchest pain, aggravated by bending forward,
squatting and lying down (positions that facilitate exposure to acid); occurs after consumption of spicy
foods, hot liquids or alcohol
— Regurgitation of food and acid in the oral cavity is especially favored by bending the body forward or
lying down
— Dysphagia - occurs in about 1/3 of patients and most often suggests a peptic stenosis

Positive diagnosis

— Positive diagnosis - clinical diagnosis - typical symptoms in patients under 45 years

— Initial assessment - presence, severity, frequency of heartburn, regurgitation and warning signs (weight
loss, dysphagia, odynophagia, haemorrhage, dysphonia, lymphadenopathy, etc.) + risk factors
— Therapeutic test (PPI 40 mg x2 / day, 1 week) - not formally recommended, but frequently used

Investigations

q Testing for H pylori infection - even if no positive correlation has been shown between H pylori and
GERD, testing is recommended in high prevalence countries
q Barium swallow - indicated in the presence of dysphagia
q Esophageal manometry - has no diagnostic role; indicated preoperatively or in patients with persistent
symptoms
q Esophageal ph-metry - useful if there is no response to PPIs; recommended to confirm reflux before
surgery;
- consists of inserting a nasogastric tube with a pH sensor, which is placed in SEI; allows measurement of acid
exposure
- the Bravo capsule (wireless probe) is attached to the lower esophagus without the need for a nasogastric tube

q Upper GI endoscopy
- indicated in cases with alarm symptoms or in cases who don’t responde to treatment
- allows the evaluation of esophagitis and hiatal hernia
- Reflux esophagitis - present in 30-50% of patients with GERD examined endoscopically
 Los-Angeles Classification
Grade A – one/more erosions < 5 mm
Grade B – at least one loss of substance >
5mm, non-confluent
Grade C – at least one lossof substance
extendend between 3 or 4 mucosal fold
Grade D – circumferential loss of substance
Savary-Miller Classiffication
1 – non-confluent eritematous erosions, one or
more
2 – multiple confluent, non-circumferential
erosions
3 – confluent, circumferential erosions
4 –complications (ulcer, Barrett esophagus,
stenosis)

Differential diagnosis

— Esophagitis – other causes — Ulcer

— Achalasia — Functional pirosis
— Esophageal cancer — Angina
— Diffuse esophageal spasm

Therapeutic principles
• Diet - small meals quantitatively, repeated; raising the head of the bed at an angle of 15 degrees or 15-20
cm; avoidance of clinostatism for 3 h postprandial; weight loss; Avoid consumption of: fat, tobacco,
alcohol, coffee, chocolate, citrus, mint, spices, sour drinks, tomato juice
• Medical treatment
• Surgery

Medical treatment

o Antiacids
o neutralizes HCl, relieves symptoms
o are used in mild forms of the disease
o alginate antiacids form a gel / film with gastric contents, reducing the aggressiveness of acid
reflux
o Magnesium-containing antacids tend to cause diarrhea, while aluminum-containing compounds
can cause constipation
o short-term effect -> is administered 3-4 times / day
o Prokinetic agents (metoclopramide and domperidone) - may improve peristalsis and accelerate gastric
emptying; are rarely used in the treatment of GERD
o H2 receptor antagonists (cimetidine, ranitidine, famotidine and nizatidine) - commonly used. They can
be used in combination with PPIs for patients with more severe forms of GERD
o Proton pump inhibitors (omeprazole, rabeprazole, lansoprazole, pantoprazole, esomeprazole)
o -inhibits adenosine triphosphatase hydrogen / gastric potassium
o -PPI reduces gastric acid secretion by up to 90%
o -election treatment for GERD; effective in refractory esophagitis
o -used in the treatment of extraesophageal manifestations of GERD, as well as in cases of peptic
esophageal stenosis
 PPI Dosage
Recommended Mild/medium forms Severe forms
doses for PPI Omeprazole 20-40 mg/day 40 mg x 2/day
treatment:
Lansoprazole 30 mg/day 30 mg x 2/day
Pantoprazole 20-40 mg/day 40 mg x2/day
Rabeprazole 20-40 mg/day 40 mg x2/day
Esomeprazole 40 mg/day 40 mg x2/day
Strategy:
Ø Rare symptoms (1-2 times/week) -> diet + antiacids +/- prokinetic agents
Ø Medium symptoms, negative gastroscopy/ grade A / B -> standard dose H2 receptor antagonists or PPI
blockers
Ø Severe symptoms, esophagitis grade C / D -> IPP standard dose; double dose 8 weeks in case of inefficiency

Step therapy:
Ø step-down: PPI standard dose 6-8 weeks -> dose reduction or switching to other classes of drugd
Ø step-up: antacids / prokinetics or H2R blockers -> PPIs in case of inefficiency; the most accepted

Refractory esophagitis (persistent symptoms after 8 weeks of double-dose PPI therapy): add antiH2 in the
evening or administer Dexlansoprazole (next-generation of PPI) -> has the strongest antisecretory effect

Surgical treatment
Indications:
- GERD complications
- lack of response to medical treatment
- severe extradigestive manifestations
- large hiatal hernia
Current surgical techniques (Nissen, Toupet) restore the esogastric junction to the abdominal cavity, mobilize
the gastric fornix, close the diaphragmatic leg and perform a short, stress-free fundoplication.
The laparoscopic Nissen fundoplication has a success rate of over 90% at 5 years

The Linx reflux management system consists of a row of magnets that increase the closing pressure of the SEI,
allowing food to pass through during swallowing; it is placed laparoscopically

GERD Complications

Ø Reflux esophagitis
Ø Benign esophageal stenosis
Ø Barrett’s sindrome (premalignant lesion with risk of developing esophageal ADK; distal esophagus
covered with columnar epithelium per min 1 cm + intestinal metaplasia with goblet cells)
Ø Esophageal adenocarcinoma
Ø Esophageal ulcer
Ø Bleeding
ACHALASIA

— esophageal motility disorder

— lack of esophageal peristalsis and impaired SEI relaxation or insufficient relaxation during swallowing
— the incidence is 1: 100,000, equal for men and women, without racial predisposition
— occurs at any age, but rarely in childhood; common in adults (30-60 years)
— higher risk in people with poor socio-economic status, in people who have pets
— protective factors - tobacco and alcohol consumption

Pathogeny
— the etiology is unknown
— autoimmune causes (associated with diseases such as psoriasis, sjogren sd), viral (achalasia has been
described more frequently in patients with varicella-zoster virus infection) or neurodegenerative etiology
— a similar clinical picture appears in chronic Chagas disease in which there is an impairment of the
neuronal plexus of the digestive tract
— histopathological examination shows inflammation of the myenteric plexus of the esophagus, with a
reduction in the number of ganglion cells. Cholinergic innervation seems urge. Immunohistochemical
examination showed a reduction in neurons containing nitric oxide synthetase. Pharmacological studies
in achalasia patients advocate selective loss of inhibitory neurons

Symptomatology
o The most common symptoms:
ü Dysphagia ü Heartburn
ü Atypical chest pain ü Weight loss
ü Regurgitation
o Frequently confused with GERD -> diagnosis may be delayed up to 2 years
o Long history of intermittent dysphagia, for both fluids and solids, from onset. At the same time,
regurgitation occurs, which contains food from the dilated esophagus, especially at night, which can
cause aspiration pneumonia as a complication of the disease. There is also spontaneous chest pain,
which is considered a consequence of esophageal "spasm", which can be misdiagnosed as cardiac pain.
Minimal weight loss.

Investigations

Upper GI endoscopy
ü The first investigation required in patients with dysphagia
ü In the early stages of disease: punctiform cardia, resistance to the passage of the endoscope
ü In progressive forms of the disease: dilated esophagus, retention esophagitis (inflammatory
lesions of the mucosa due to food stagnation), food or liquid waste

Chest X-ray shows:

ü Mediastinum enlarged due to the much dilated esophagus
ü Mediastinal hydroaerial level
ü Absence of stomach gas bubble (lack of SEI relaxation does not allow air to pass into the
stomach)
Barium swallow shows:
 ü lack of peristalsis
ü synchronous contractions of the esophageal body, sometimes associated with its dilation
ü appearance of a "bird's beak of the distal end of the esophagus, caused by insufficient relaxation
of the SEI
Manometry:
ü It shows the absence of esophageal peristalsis
ü Highlights the absence of SEI relaxation during swallowing by assessing the integrated
relaxation pressure (IRP)
ü High resolution manometry is the gold standard for confirming the diagnosis of achalasia

Chicago Type I Achalasia Type II Type III Achalasia

classification of Achalasia
achalasia: IRP >15 mmHg >15 mmHg >15 mmHg
Contractions absent absent ≥20% premature
Differential apearreance contractions
diagnosis Panesophageal ≥20% from
— Secondary pressurisation swallows
achalasia / (>30 mmHg)
pseudo-
achalasia (by mechanical compression of the lower esophageal sphincter or infiltration of LES)
— Diffuse esophageal spasm
— Hyperkinetic esophagus
— Lower esophageal sphincter hypertrophy
— Amiloidosis
— Sarcoidosis
— Scleroderma

Treatment Therapeutic options:

Objectives: • Adjuvant pharmacological treatment
— Decreased esophageal resting tonus • Endoscopic dilation
— Improvement of esophageal emptying • Botulinum toxin injection
— Improvement / cancellation of symptoms • Myotomy (surgical, laparoscopic, robotic)
• New approaches: POEM, stenting
q Pharmacological treatment:
— The least efficient
— Short-term effects
— Nitrates (isosorbide dinitrate), calcium channel blockers (Verapamil, Nifedipid 10-20 mg sublingual)
— Indicated in patients refusing endoscopic / surgical treatment

q Botulinum toxin injection:

— Neurotoxin that blocks the release of acetylcholine at the synaptic terminals -> relaxation of the
esophageal muscle fibers of cardia
— Indicated in patients with incipient forms, elderly, patients with high risk for surgery

Endoscopic dilation
— With Rigiflex probes
— Involves standard radiological care
— Requires sedation
— The efficiency can be assessed clinically, radiologically and manometrically
— Indicated for the elderly, those at surgical risk or those who refuse surgery
 — A maximum of 3 sessions are held: in case of failure -> surgical myotomy

Surgical treatment- Heller miotomy:

- In young people, or in those whose endoscopic maneuvers have failed
- The cardial esophageal muscles are sectioned

POEM (peroral endoscopic myotomy)

— A breach is made in the mucosa, then saline and methylene blue are injected into the submucosa to
create a workspace.
— Circular fibers are cut from the lower esophagus, cardia and 2-3 cm subcardially

Esophageal stenting
— With self-expanding metal stent
— It is not a long-term treatment

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