3. INTRODUCTION
➢ It has an upper and a lower esophageal sphincter.
➢ The mucosa is lined by nonkeratinizing stratified
squamous epithelium.
➢ It functions to transport food and fluid to the
stomach, otherwise remaining empty.
➢ The esophagus is a muscular tube that extends
25 cm from the cricoid cartilage to the cardiac
orifice of the stomach.
5. Gastro-oesophageal refux disease
• Gastro-oesophageal reflux resulting in heartburn affects
approximately 15% of the general population.
• Pathophysiology: Gastro-oesophageal reflux disease develops
when the oesophageal mucosa is exposed to gastroduodenal
contents for prolonged periods of time, resulting in symptoms
and, in a proportion of cases, esophagitis.
• Several factors are known to be involved in the development of
gastro-oesophageal reflux disease
6.
7. Clinical Features
• Heart burn and regurgitation are major symptoms
• Waterbrash
• Night choking
• Odynophagia/ Dysphagia
• Atypical chest pain ( reflux induced oesophageal
spasm)
• Hoarseness (acid laryngitis)
• Recurrent chest infections
• Chronic cough
8. Investigations
• Endoscopy is the investigation of choice
• Investigation is advisable if patients present over the
age of 50–55 years, if symptomsare atypical or if a
complication is suspected.
• Oesophageal pH monitoring is indicated if the
diagnosisis unclear or surgical intervention is under
consideration (An oesophageal pH of less than 4 for
more than 6% of the study time is considered
diagnostic for reflux disease).
9. Management
Lifestyle advice:
• weight loss
• avoidanceof dietary itemsthat worsen symptoms
• elevation of the bed head in those who experience
nocturnal symptoms
• avoidanceof late meals
• cessation of smoking.
10.
11. Complications of GERD
➢ Oesophagitis
➢ Iron deficiency anaemia: It can
occur as a consequence of occult
blood loss from long-standing
oesophagitis.
12. Complications of GERD
➢ Benign oesophageal stricture:
Fibrous strictures can develop as a consequenceof longstanding
oesophagitis.
Presentation: Dysphagia that is worse for solids than for liquids.
Diagnosis: Endoscopy and biopsy
Treatment: Endoscopic balloon dilatation or bouginageis helpful and
long term PPI therapy at full dose.
13. Complications of GERD
➢ Gastric volvulus
Occasionally, a massive intrathoracic hiatus hernia may
twist on itself, leading to a gastric volvulus.
Presentation: Severe chest pain, vomiting and
dysphagia.
Diagnosis: Chest X-ray (air bubble in the chest) and
barium swallow.
Treatment: Nasogastric tube decompression and
surgery.
14. Complications of GERD
➢ Barrett’soesophagus:
A pre-malignant condition, in which the normal squamous lining of
the lower oesophagus is replaced by columnar mucosa.
Patients are often asymptomatic until discovered, and can present
with oesophageal cancer.
The estimated prevalence in Western countries is 1%–2% of the
population.
It’s more common in men, obese, and those over 50 years of age.
16. • Neither potent acid suppression nor anti-reflux surgery stops
progression or induces regression of Barrett’s oesophagus, and
treatment is indicated only for symptoms of reflux or complications,
such as stricture.
• Endoscopy: 3-5 yearly intervals if the Barrettic segment is less than
3cm, 2–3 yearly intervals if the length is greater than 3 cm, 6 monthly
interval if low-grade .
• Patients with high grade dysplasia or intramucosal carcinoma should
be treated with oesophagectomy or endoscopic therapy.
Management:
18. As a result of the increased use of immunosuppression for
organ transplantation and chronic inflammatory diseases and
use of chemotherapy agents, along with the AIDS epidemic,
infections with Candida species, herpesvirus, and
cytomegalovirus (CMV) have become relatively common.
Presentation:
Odynophagia, dysphagia, chest pain, hemorrhage.
Infectious Oesophagitis
19. Infectious Oesophagitis
➢ CANDIDIA ESOPHAGITIS
• Candida is normally found in the throat but can
become pathogenic and produce esophagitis in a
compromised host; C. albicans is most common.
• Candida esophagitis also occurs with esophageal
stasis.
• Endoscopy: white plaques or exudate with friability.
• Treatment: Empirical therapy is appropriate if oral
thrush is present but co-infection is
common.Fluconazole ( 200mg daily oral/IV for 14
days)
20. Infectious Oesophagitis
➢ HERPETIC ESOPHAGITIS
• Herpes simplex virus type 1 or 2 may cause
esophagitis. Vesicles on the nose and lips may
coexist and are suggestive of a herpetic etiology.
• Varicella-zoster virus can also cause esophagitis in
children with chickenpox or adults with zoster.
• Endoscopy: vesicles and small, superficial
ulcerations.
• Treatment: Acyclovir (200 mg orally five times daily)
In patients with severe odynophagia ( IV acyclovir, 5
mg/kg every 8 h for 7–14 days)
21. Infectious Oesophagitis
➢ CYTOMEGALOVIRUS
• CMV esophagitis occurs primarily in immunocompromised patients,
particularly those with HIV, patients with malignancy, and recipients of bone
marrow or organ transplants.
• CMV is usually activated from a latent stage.
• Endoscopy: CMV lesions appear as large serpiginous ulcers in an
otherwise normal mucosa, particularly in the distal esophagus.
• Treatment: Ganciclovir (5 mg/kg every 12 h IV) and valganciclovir (900 mg
orally every 12 h). - Therapy is continued until healing, which may take 3–6
weeks.
22. Corrosive Esophagitis
• Suicide attempt by ingestion of strong household bleach
or battery acid is followed by painful burns of the mouth
and pharynx and by extensive erosive oesophagitis.
• Late complications include oesophageal strictures, which
may require endoscopic dilatation or stent insertion, or
surgery in severe cases.
23. Pills Esophagitis
• Pill-induced esophagitisoccurs when a swallowed pill fails to
traverse the entire esophagus and lodges within the lumen.
• Attributed to Poor pill-taking habits.
• The mostcommon location for the pill to lodge is in the mid-
esophagus near the crossing of the aorta or carina. Extrinsic
compression from these structures halts the movement of the
pill or capsule.
• Pills esophagitis cal also occur when the tablets are trapped
above an oesophageal stricture.
24. Eosinophilic esophagitis
• Eosinophilic infiltration of the esophageal mucosa.
• Affects both children and adults, more common in males.
• Seen more in atopic patients
• Children commonly present with vomiting, difficulty feeding or failure
to thrive.
• Adults present with dysphagia or food bolus obstruction.
• Endoscopy: Usually normal, but mucosal rings, exudates, oedema,
strictures or a narrow-calibre oesophagus can occur.
• Histopathology: Increase in eosinophil density (≥ 15 eosinophils per
high-powered field (HPF)).
26. Eosinophilic esophagitis
Management:
• Dietary modifications: elemental and elimination diets.
• Pharmacological: Empiric 8-week trial of high-dose PPI.
• If no response to PPI: 8–12 weeks of therapy with
glucocorticoidscan be used, such as fluticasone and
budesonide.
• Endoscopic esophageal dilatation for patients with strictures or
mucosal rings that have failed to respond to medical therapy.
28. Achalasia
Is a disease entity of unknown etiology Characterized by
absence of peristalsis in the body of the esophagus, a high
resting pressure at the (LES) and failure of this sphincter to
relax in response to swallowing
• Pathology :In achalasia , the body and the upper segment of
the esophagus becomedilated, tortuous& hypertrophied
.The most specific histological abnormality found by
(Electron Microscope) is the degeneration or disappearance
of the ganglion cells of the Auerbach’s plexus.
29. Achalasia
Clinical features
The presentation is with dysphagia.
This develops slowly, is initiallyintermittent, and is worse for solids and
eased by drinking liquids and by standing and moving around after
eating.
Heartburn does not occur because the closed oesophageal sphincter
prevents gastro-oesophageal reflux.
Some patients experience episodes of chest pain due to oesophageal
spasm.
As the disease progresses, dysphagia worsens, the oesophagus empties
poorly and nocturnal pulmonaryaspiration develops. Achalasia
predisposes to squamous carcinoma of the oesophagus.
30. Achalasia
Diagnosis :
1) CXR : Absence of gastric air bubble, Visible Esophagus.
2) Barium Swallow x-ray : “Diagnostic” Dilated Esophagus ,full
of barium , Normal mucosal lining ,food residue, Little
barium passed to the stomach. Morphological forms
:Cucumber ,Tortuous & Sigmoid Bird’s beak appearance
3) Endoscopy with biopsy : To rule out malignancy and to
exclude other path.
4) Manometry : Absence of peristalsis(body), high LES
pressure(impaired relaxation)
31. Achalasia
Treatment
• Surgery : Heller’scardio myotomy
➢Thoracic approach
➢Abdominal approach
• Recently Laparoscopic cardio myotomy
• Dilatation : pneumaticor hydrostaticballoon Dilation.
• Medical treatment : by calcium channel blockers (adalat) ,
and nitrate (isordil).
32.
33. Complications Achalasia
1) Those related to retention & stasis ( Retention esophagitis )
2) Air way obstruction & repeated chest infection.
3) Pre malignant (squamous cell carcinoma )
35. Diffuse esophageal spasm (DES)
Also known as distal esophagus spasm, is a condition
characterized by uncoordinated contractions of the esophagus,
which may cause difficulty swallowing (dysphagia) or
regurgitation.
In some cases, it may cause symptoms such as chest pain ,
similar to heart disease.
In many cases, the cause of DES remains unknown.
Pathophysiology : Uncoordinated, simultaneous contractions of
esophageal body
36. Diffuse esophageal spasm (DES)
Signs and symptoms
• DES manifests as intermittent difficultyswallowing solid
foods and liquids (dysphagia), and atypical chest pain.
• The chest pain may appear similar to cardiac chest pain
(angina pectoris), so investigating the possible existence of
heart disease is often indicated.
38. Diffuse esophageal spasm (DES)
Treatment
1) Medical : Calcium channel blockers.
Alternates: Nitrates or tricyclics.
2) Surgical : Myotomy is effective for Treating
diffuse esophageal spasm. Themyotomy
should extend the entire length of the
involved segment, which should be
determines preoperatively with manometry.
40. Systemic sclerosis
• Sclerodermais a group of autoimmunediseases that may result
in changes to the skin, blood vessels, muscles, and internal
organs.
• The disease can be either localized to the skin or involve other
organs, as well .
• Symptoms may include areas of thickened skin, stiffness,
feeling tired , and poor blood flow to the fingersor toes with
cold exposure.
• One form of the condition, known as CREST syndrome,
classically results in Calcium deposits, Raynaud's phenomenon,
Esophageal dysmotility, Sclerodactyly, and Telangiectasia.
41. Systemic sclerosis
• Pathophysiology: Since smooth muscle is targeted in the
pathologyof SSc, the lower two-thirds of the esophagusand
lower esophageal sphincter (LES) are atrophyand fibrosis , as
the upper third of the esophagus is primarily composed of
skeletal muscle .
• symptom : typicallyincludes dysphagia, pseudo-obstruction,
regurgitation, heartburn, nausea or vomiting, all of which can
lead to poor eating and severe weight loss , Esophageal
dysfunction permits gastric reflux
42. Systemic sclerosis
• Diagnosis
➢ Ba swallow : normal
➢ EGD and biopsy : atrophy and fibrosis
➢ Manometry : decreased motility at mid distal esophagus &
decrease LES pressure
• Management
➢ PPI : to reduce risk of reflux esophagitis.
44. HIATAL HERNIA
• Hiatal hernia is a herniation of viscera, most commonly the stomach, into the
mediastinum through the esophageal hiatus of the diaphragm.
• The etiology Is multifactorial
➢ Lax diaphragmatic esophageal hiatus
Advanced age
Smoking
Obesity
Genetic predisposition (rare)
➢ Prolonged periods of increased intra-abdominal pressure
Pregnancy, Ascites, Chronic cough, Chronic constipation
46. Type I: sliding hiatal hernia
Most common type (95% of cases), The GEJ and the gastric cardia slide
up into the posterior mediastinum.
Type II
Part of the gastric fundus herniates into the thorax. The GEJ remains in
its anatomical position below the diaphragm.
47. Type IV: complex hiatal hernia
Herniation of any abdominal structure other than the stomach (e.g., spleen,
omentum, or colon)
Type III: mixed hiatal hernia
Mix of types I and II
▪ Type II, III, and IV hiatal hernias are all subtypes of paraesophageal
hernia
48. Clinical features
Most patients are asymptomatic
Type I: symptoms of GERD
Type II, III, and IV
Epigastric/substernal pain, Early satiety, Retching,
Symptoms of GERD can occur.
51. . Conservative management:-
Lifestyle modifications, Proton pump inhibitors (PPIs) or histamine H2-receptor
antagonists in sliding (type I) hiatal hernia
. Surgery :- Nissen ‘s fundoplication (lapratomy or laparascopic)
Indication:-types II, III, IV hiatal hernias
No indication for type I unless severe symptoms/complications.
Treatment
52. are abnormal pouches that arise from the wall of the esophagus.
. Middle esophageal diverticulum: diverticulum at the tracheal bifurcation
. Lower esophageal diverticulum: epiphrenic diverticulum
. Upper esophageal diverticulum:- Most common type: Zenker diverticulum at
the Killian triangle
Classification
-according to Localization:-
Esophageal diverticula
53.
54. - according to histology :-
False diverticula: Increased intraluminal pressure causes only the mucosa
and submucosa to bulge through weak points in the muscularis (e.g., in
Zenker diverticulum).
True diverticula: All layers of the esophageal wall protrude.
55. Upper esophageal diverticula (e.g., Zenker diverticulum)
Most patients report some degree of dysphagia.
Additional symptoms can include:
Regurgitation of undigested food
Halitosis
Aspiration pneumonia
Clinical features
Middle esophageal and epiphrenic diverticula
Patients usually remain asymptomatic.
Associated symptoms are often attributable to the underlying disorder (e.g.,
achalasia causing chest pain and/or dysphagia).
Some notice gurgling in throat after swallowing
56. -Barium swallow with videofluoroscopy
the first-line test for diagnosing esophageal diverticula
-Endoscopy and Esophageal manometry indicates in patients with middle and
lower esophageal diverticula
Diagnostics
57. -Zenker diverticulum
Procedures: based on diverticulum size and the chosen approach (i.e.,
endoscopy or open surgery)
. Diverticulotomy
. Diverticulectomy
. Diverticulopexy
-Other diverticula
If symptomatic or diverticulum ≥ 2 cm: Consider surgical intervention (e.g.,
diverticulopexy).
Treatment
58. circumferential filling defect typically arising from
the distal esophageal wall one of the most
common causes of intermittent food impaction
Symptomatic rings are readily treated by dilation.
Schatzki rings:-
RINGS AND WEBS
59. Esophageal web:-
small (1–2 mm) filling defect arising from the proximal
esophageal wall
Can also cause intermittent dysphagia to solids and are
similarly treated with dilation
combination of symptomatic proximal esophageal webs
and iron-deficiency anemia in middle-aged women
constitutes Plummer-Vinson or Paterson-Kelly
syndrome.
61. Benign tumours
Benign esophageal tumors are uncommon and usually discovered incidentally. In
decreasing frequency of occurrence, cell types include leiomyomas, fibrovascular
polyps, squamous papillomas, granular cell, lipomas, neurofibromas, and
inflammatory fibroid polyps. These generally become symptomatic only when they
are associated with dysphagia and merit removal only under the same circumstances.
62. Esophageal cancer
Esophageal cancer (EC) is the eighth most common type of cancer worldwide
and affects men more than women (3:1 ratio). It is found commonly in people
in 60-70 yrs old ..
The two main forms are esophageal adenocarcinoma and squamous cell
carcinoma. Esophageal adenocarcinomas are among the neoplasms with the
fastest increasing incidence in northern and western Europe and North
America, while squamous cell carcinoma is the most common form
worldwide.
63. Adenocarcinoma, which usually affects the
lower third of the esophagus, may be preceded
by gastroesophageal reflux disease and Barrett
esophagus. Other risk factors include smoking
and obesity. Risk factors for squamous cell
carcinoma include carcinogen exposure (e.g., in
the form of alcohol and tobacco) and a diet high
in nitrosamines but low in fruits and vegetables.
the overall 5-year survival of patients presenting
with oesophageal cancer is only 13%.
64. • Painless, rapidly progressive dysphagia is classic.
• Odynophagia
• Weight loss.
• Chest pain (usually late, suggests local invasion).
• Hoarse voice (usually late, suggests local
invasion).
• Coughing after swallowing, pneumonia or pleural
effusion suggests esophagobronchial fistula.
• Acutely: bolus obstruction.
• Examination may be normal until late – look for
cervical nodes.Dysphagia is the most common
presenting symptom, but is a late feature
Clinical features
65. • Upper GI endoscopy with biopsy: demonstrates
site and allows histological sampling.
• Barium swallow: demonstrates length of stricture
if the tumor could not be intubated at endoscopy.
• CT of the thorax and abdomen: for staging.
• Endoscopic ultrasound: best staging modality.
• Positron emission tomography/computed
tomography (PET-CT) demonstrating a primary
tumour and a distant metastatic node.
Investigations
Endoscopic view of Esophageal cancer
Barium swallow
66. Management
The treatment of choice is surgery if the patient presents at a point at which
resection is possible.
• Endoscopic submucosal resection for mucosal lesions .
• Subtotal or total esophagectomy Chemoradiotherapy • Neoadjuvant
Chemoradiotherapy
• Chemoradiotherapy with or without targeted therapiesOther interventional
therapy
• Endoscopic placement of self-expanding metal stents for palliation of
dysphagia and fistulae
• Gastrojejunostomy (GJ) tube for specialized nutrition support
67. Perforation of the esophagus
Oesophageal perforation is associated with high morbidity and mortality rates.
Aetiology
1-Traumatic perforation following instrumentation like rigid esophagoscope, Foreign
bodies ingestion or blunt and penetrating trauma
2-Spontaneous rupture ( Boer-haave’ s syndrome ) due to the strian of emesis with
or without predisposing disease .
3-Corrosive ingestion, Eosinophilic oesophagitis, Oesophageal cancer.
Perforation may also result at the site of stricture in the setting of endoscopic food
disimpaction or esophageal dilation.
68. Clinical manifestations :
Esophageal perforation causes severe pleuritic retrosternal pain and
shock occur as oesophago-gastric contents enter the mediastinum and
thoracic cavity. that can be associated with pneumomediastinum and
subcutaneous emphysema. Mediastinitis is a major complication of
esophageal perforation, and prompt recognition is key to optimizing
outcome.
70. Treatment
Treatment includes nasogastric suction and parenteral broad-
spectrum antibiotics with prompt surgical drainage and repair in
noncontained leaks. Conservative therapy with NPO status and
antibiotics without surgery may be appropriate in cases of minor
instrumental perforation that are detected early. Endoscopic
clipping or stent placement may be indicated in nonoperable cases
such as perforated tumors.
