Surgical disease of the esophagus

Mahteme Bekele ,MD

Assistant professor of surgery
Presentation outline
Common disorders of the esophagus
Investigation modalities used in esophageal disorder
Specific diseases
Esophageal carcinoma
Achalasia
GERD
stricture

Anatomy of the esophagus
The esophagus is about 25 cm long, extending from
the level of the sixth cervical vertebra down to that of
the 11th thoracic vertebra.
There is a narrowing at 15 to 17 cm, the upper
esophageal sphincter; another at about 38 to 40 cm, the
lower esophageal sphincter; and an anterolateral
indentation at about 25 cm where the left main
bronchus and arch of the aorta cross it anteriorly
Anatomy
 Three physiologic constrictions:
Cricopharyngeal 15cm
Aortic and bronchial 25cm
Diaphragmatic 40cm

Importance:
 Foreign body lodgment
 Perforation during endoscopy
 Malignancy
Esophageal diseases
I: Neuro-muscular
 Inadequate LES relaxation
• Achalasia
• Epiphrenic diverticulum

 Uncoordinated esophageal contraction

• Diffuse esophageal spasm (DES)

 Hypo-contarction
• Ineffective esophageal motility (IEM)
Esophageal diseases
 Hyper-contraction
 High-amplitude peristaltic contraction (HAPC,
“nutcracker esophagus”),
II. Inflammatory
 Reflux esophagitis
 Caustic esophagitis
 Infectious esophagitis
 Foreign body
Esophageal diseases

III: Anatomic:
Sliding hiatus hernia
Rolling (Para-esophageal) hiatus hernia
Mixed hiatus hernia
Esophageal diverticular diseases

IV: Neoplastic
Esophageal carcinoma
Benign tumors
 Differential diagnosis of dysphagia
 With in the lumen
o Foreign body
o mucosal polyps, lipomas, fibrolipomas, or myxofibromas
 On the wall
o Stricture : Caustic stricture , secondary to esophagitis and reflux,
tuberculous
o Esophageal ca
 o Esophageal Webs
o Esophgeal diverticulum eg. Zenker‘s
o Muscular spasm: diffuse esophgeal spasm,
achalesia (ganglionic dysfunction)
o Tetanus
 Outside the wall
o Thyroid swelling
o Cardiomegally
o Mediastinal mass
o Hiatal hernia
 Clinical feature
• History
– Dysphagia
• Acute: foreign body in children, tonsilopharyngitis
• Chronic solid then liquid in ca reverse in achalesia
– Odynophagia : esp. diffuse esophageal spasm
– Regurgitation and weight loss : fast in ca
– respiratory symptoms caused by aspiration are present.
– chest pain, which can radiate to the back, neck, ears, jaw, or arms and may be
confused with typical angina pectoris in chest pain, which can radiate to the
back, neck, ears, jaw, or arms and may be confused with typical angina
pectoris
– tobacco use, excessive alcohol ingestion, nitrosamines, poor dental hygiene,
and hot beverages. Certain pre-existing conditions including achalasia and
Barrett's esophagus
• No typical p/E
Investigations
 barium swallow reveals a localized smooth filling defect in the
esophageal wall.
 Esophagoscopy is performed to confirm the diagnosis not in
suspected diverticulum to avoid perforation
 Biopsy of the lesion
 Endoscopic ultrasound (EUS)
 Manometry:in achalesia; spasm
 Computed tomography (CT) scan
Treatment
 Dilatation
 Myotomy: opening on muscle in acalesia(modified Heller
procedure), diverticulum
 Diverticulectomy
 F.B removal
 Resection
 Chemoradiotherapy
 muscle relaxants, such as nitrates;botulinim toxin
Esophageal Cancer: Introduction

 Causes 1-2% of all cancer related deaths

 Most occur above 50 years of age

 M:F = 3:1

 Common in Ethiopia

 Causes death due to starvation and dehydration

Esophageal Cancer: Risks and causes
1. Chronic alcohol consumption

2. Chronic smoking and tobacco chewing

3. Diets high in nitrites or nitrosamines

4. Spicy foods with spirits

5. Frequent very hot diet

 Pre-cancerous conditions

1. Achalasia

2. Corrosive stricture

3. Plummer-vinson syndrome with squamous metaplasia

4. Reflux esophagitis with barret’s esophagus

Esophageal cancer: Sites
 Middle 1/3: 50%
 Lower 1/3: 33%
 Upper 1/3: 17%

 Histology
1. Squamous cell carcinoma: More common in Ethiopia

2. Adenocarcinoma
Esophageal Cancer: Symptoms
 Gradual onset of dysphagia first for solids, then for both
liquids and solids, then to saliva

 Anorexia and odenophagia

 Profound weight loss, weakness

 Rarely, features of metastasis

Esophageal cancer: signs
 In early disease: may be entirely normal

 Cachexia, dehydration and shock

 Cervical and supra-clavicular LAP

 Rarely, features of metastasis

Esophageal Cancer: Staging
Staging
T1: invades lamina propria or sub mucosa
T2: invades muscularis propria
T3: invades adventitia
T4: invades adjacent structures

N0: no lymph nodes

N1: regional lymph nodes

M1: distant metastasis, including celiac or cervical nodes

Esophageal Cancer: Staging
Stage I : T1 N0

Stage 2A: T2 N0 and T3 N0

Stage 2B: T1 N1 and T2 N1

Stage 3 : T3 N1 and T4 any N

Stage 4 : M1
Esophageal Cancer: Investigation

 Esophagoscopy and biopsy: Gold standard

 Endo-esophageal ultra sound

 Barium swallow

 CT- Scan

 Abdominal ultrasound
Treatment
Esophagectomy: Surgery

Chemotherapy

Radiotherapy
Achalasia
 Achalasia (“failure to relax"): loss of peristalsis in the
distal esophagus and a failure of LES relaxation.

 The etiology of achalasia is not known

Autoimmune disorder - associated with HLA-DQw1

antibodies to enteric neurons

Chronic infections with herpes zoster or measles

viruses.

Chaga’s disease
 Achalasia: Pathology
 Ineffective relaxation of the LES

 loss of esophageal peristalsis → impaired

esophageal emptying and gradual dilatation

 Decrease or loss of myenteric ganglion cells

 Slight increase risk of esophageal carcinoma

PATHOPHYSIOLOGY

PATHOPHYSIOLOGY
Achalasia
Incidence
 Annual incidence of approximately 1 case per 100,000.

 Men and women are affected with equal frequency.

 Usually diagnosed between the ages of 25 and 60 years.

 Seen and reported from Ethiopia.

 Beware of pseudo-achalasia
Symptomatology

 Dysphagia: delayed (about 2 years) and progressive,

worse for fluid than solid,

 Weight loss

 Regurgitation of undigested food

 Regurgitation associated pulmonary complication

 Chest pain
Achalasia: Investigations
 CXR: Esophageal air fluid levels

 Barium swallow: Dilated esophagus with Bird's beak

deformity.

 Manometry: gold standard

Elevated LES pressure (> 35mmHg)
 Incomplete sphincter relaxation
 Complete absence of peristalsis

 Endoscopy: dilated esophagus with tightly closed LES

→ gentle pressure will admit the scope with a "pop“.
Achalasia: Pseudo-achalasia
Achalasia: Treatment
 Palliation of dysphagia is the key:
→ relieve functional obstruction of distal esophagus

Options of treatment
 Pharmacotherapy
 Botulinum toxin
 Esophageal dilation
 Operative myotomy (Heller’s cardiomyotomy)
Achalasia: Pharmacotherapy

 Nitrates

 Ca++ channel blockers

 Anticholinergics

 Opiods
Botulinum Toxin injection
Baloon dilatation
Modified Heller’s cardiomyotomy
Gastroesophgeal reflux disease
 Definition

Symptoms OR mucosal damage produced

by the abnormal reflux of gastric contents
into the esophagus
Often chronic and relapsing
Physiologic vs Pathologic
Physiologic GERD Pathologic GERD
Postprandial Symptoms
Short lived Mucosal injury
Asymptomatic Nocturnal sx
No nocturnal sx
Epidemiology
accounts for approximately 75% of esophageal
pathology
About 44% of the US adult population have heartburn
at least once a month
Pathophysiology
 Primary barrier to
gastroesophageal reflux is
the lower esophageal
sphincter
 LES normally works in
conjunction with the
diaphragm
 If barrier disrupted, acid
goes from stomach to
esophagus
From an anatomic–surgical point the antireflux
mechanism is based on the following elements

Thickening of the gastric oblique sling fibers and the

clasp fibers that form the lower esophageal sphincter
Intra-abdominal pressure
Rosette-like configuration of the top end of the gastric
mucosal folds
The sharp angle of the fundus (angle of His)
The phrenoesophageal membrane and its insertion into
the esophagus
The pinching of the diaphragmatic crura
Clinical Manisfestations

 Most common symptoms

 Heartburn—retrosternal burning discomfort
 Regurgitation—effortless return of gastric
contents into the pharynx without nausea,
retching, or abdominal contractions
Clinical Manisfestations
Dysphagia—difficulty swallowing
Other symptoms include:
 Chest pain, water brash, globus sensation, odynophagia, nausea
Extraesophageal manifestations
 Asthma, laryngitis, chronic cough
Diagnostic Evaluation
If classic symptoms of heartburn and regurgitation exist
in the absence of “alarm symptoms” the diagnosis of
GERD can be made clinically and treatment can be
initiated
Alarms
Alarm Signs/Symptoms
 Dysphagia
 Early satiety
 GI bleeding
 Odynophagia
 Vomiting
 Weight loss
 Iron deficiency anemia
Trial of Medications
H2RA or PPI
Expect response in 2-4 weeks
If no response
 Change from H2RA to PPI
 Maximize dose of PPI
Trial of Medications
If PPI response inadequate despite maximal dosage
Confirm diagnosis
 EGD
 24 hour pH monitor
 Esophagogastrodudenoscopy
 Endoscopy (with biopsy if needed)
 In patients with alarm signs/symptoms
 Those who fail a medication trial
 Those who require long-term tx
 Lacks sensitivity for identifying
pathologic reflux
 Absence of endoscopic features does
not exclude a GERD diagnosis
 Allows for detection, stratification,
and management of esophageal
manisfestations or complications of
GERD
pH
24-hour pH monitoring
Accepted standard for establishing or excluding presence
of GERD for those patients who do not have mucosal
changes
Trans-nasal catheter or a wireless, capsule shaped device
 Patient with heartburn

Iniate tx with H2RA or PPI

H2RA taken PPI taken QD

BID
No
Good response
No
Good response Yes Yes
Yes
Maintenance therapy Increase to
Frequent relapses max dose QD
with lowest effective dose
or BID
No
Yes
On demand tx
Symptoms persist Good response
No

Consider EGD if
Confirm diagnosis
risk factors present
EGD, ph monitor
(> 45, white, male
and > 5 yrs of sx)
GERD vs Dyspepsia
Distinguish from Dyspepsia
Ulcer-like symptoms-burning, epigastric pain
Dysmotility like symptoms-nausea, bloating, early
satiety, anorexia
Distinct clinical entity
In addition to antisecretory meds and an EGD need to
consider an evaluation for Helicobacter pylori
Treatment
Goals of therapy
Symptomatic relief
Heal esophagitis
Avoid complications
Better Living
 Lifestyle modifications
 Avoid large meals
 Avoid acidic foods (citrus/tomato), alcohol, caffiene, chocolate, onions, garlic,
peppermint
 Decrease fat intake
 Avoid lying down within 3-4 hours after a meal
 Elevate head of bed 4-8 inches
 Avoid meds that may potentiate GERD (CCB, alpha agonists, theophylline, nitrates,
sedatives, NSAIDS)
 Avoid clothing that is tight around the waist
 Lose weight
 Stop smoking
Treatment
Antacids
Over the counter acid suppressants
and antacids appropriate initial
therapy
Approx 1/3 of patients with
heartburn-related symptoms use at
least twice weekly
More effective than placebo in
relieving GERD symptoms
Treatment
Histamine H2-Receptor Antagonists
More effective than placebo and antacids for relieving
heartburn in patients with GERD
Faster healing of erosive esophagitis when compared
with placebo
Can use regularly or on-demand
Treatment
AGENT EQUIVALENT DOSAGE
DOSAGES
Cimetadine 400mg twice daily 400-800mg twice daily
Tagamet

Famotidine 20mg twice daily 20-40mg twice daily

Pepcid

Nizatidine 150mg twice daily 150mg twice daily

Axid

Ranitidine 150mg twice daily 150mg twice daily

zantac
Treatment
Proton Pump Inhibitors
Better control of symptoms with PPIs vs H2RAs and
better remission rates
Faster healing of erosive esophagitis with PPIs vs
H2RAs
Treatment
AGENT EQUIVALENT DOSAGE
DOSAGES
Esomeprazole 40mg daily 20-40mg daily
Nexium

Omeprazole 20mg daily 20mg daily

Prilosec

Lansoprazole 30mg daily 15-10md daily

Prevacid

Pantoprazole 40mg daily 40mg daily

Protonix

Rabeprazole 20mg daily 20mg daily

Aciphex
Treatment
H2RAs vs PPIs
12 week freedom from symptoms
 48% vs 77%
12 week healing rate
 52% vs 84%
Speed of healing
 6%/wk vs 12%/wk
Treatment
Antireflux surgery
Failed medical management
Patient preference
GERD complications
Medical complications attributable to a large hiatal
hernia
Atypical symptoms with reflux documented on 24-hour
pH monitoring
Treatment
Antireflux surgery candidates
EGD proven esophagitis
Normal esophageal motility
Partial response to acid suppression
Treatment
Antireflux surgery
Tenets of surgery
 Reduce hiatal hernia
 Repair diaphragm
 Strengthen GE junction
 Strengthen antireflux barrier via gastric wrap
 75-90% effective at alleviating symptoms of heartburn and
regurgitation
Treatment
Postsurgery
10% have solid food dysphagia
2-3% have permanent symptoms
7-10% have gas, bloating, diarrhea, nausea, early satiety
Within 3-5 years 52% of patients back on antireflux
medications
Treatment
Endoscopic treatment
Relatively new
No definite indications
Select well-informed patients with well-documented
GERD responsive to PPI therapy may benefit
Three categories
Radiofrequency application to increase LES reflux
barrier
Endoscopic sewing devices
Injection of a nonresorbable polymer into LES area
Complications
Erosive esophagitis
Stricture
Barrett’s esophagus
Complications
Erosive esophagitis
Responsible for 40-60% of GERD symptoms
Severity of symptoms often fail to match severity of
erosive esophagitis
 Complications
Esophageal stricture
Result of healing of
erosive esophagitis
May need dilation
Complications

Barrett’s Esophagus
Columnar metaplasia of the
esophagus
Associated with the
development of adenocarcinoma
Complications
 Barrett’s Esophagus
 Acid damages lining of
esophagus and causes chronic
esophagitis
 Damaged area heals in a
metaplastic process and
abnormal columnar cells
replace squamous cells
 This specialized intestinal
metaplasia can progress to
dysplasia and adenocarcinoma
Complications
Patient’s who need EGD
 Alarm symptoms
 Poor therapeutic response
 Long symptom duration
“Once in a lifetime” EGD for patient’s with chronic
GERD becoming accepted practice
Many patients with Barrett’s are asymptomatic
Complications
Barrett’s Esophagus
Manage in same manner as GERD
EGD every 3 years in patient’s without dysplasia
In patients with dysplasia annual to shorter interval
surveillance
complication
1) mucosal complications such as esophagitis and
stricture,
 2) extra–esophageal or respiratory complications such
as laryngitis, recurrent pneumonia and progressive
pulmonary fibrosis and
3) metaplastic and neoplastic complications such as
Barrett's esophagus, and esophageal adenocarcinoma.
The prevalence and severity of complications is related
to the degree of loss of the gastroesophageal barrier,
defects in esophageal clearance and the content of
refluxed gastric juice