3. Introduction
The oesophagus is a muscular tube connecting the
pharynx to the stomach and measuring 25–30 cm in
the adult.
Its primary function is as a conduit for the passage of
swallowed food and fluid, which it propels by antegrade
peristaltic contraction.
It also serves to prevent the reflux of gastric contents
whilst allowing regurgitation, vomiting and belching to
take place
4. Anatomy of oesophagus
The oesophagus is a muscular tube protected at its ends by
the upper and lower esophageal sphincters.
Oesophagus begins at the level of the sixth cervical vertebra
and it enters into the superior mediastinum through the upper
thoracic outlet then it descends into the posterior mediastinum
and exits the thorax through oesophageal hiatus of the
diaphragm and enters the abdominal cavity
5. Anatomy of oesophagus
The esophagus is divided into three parts:-
The cervical portion extends from the
cricopharyngeus to the suprasternal notch
The thoracic portion extends from the suprasternal
notch to the diaphragm
The abdominal portion extends from the diaphragm
to the cardiac portion of the stomach.
6. Upper End : C6 (the inferior
pharyngeal constrictor merges with the
cricopharyngeus) __
Upper esophageal sphincter (UES)
Lower End: T11 (thickened circular
smooth muscle) __
Lower esophageal sphincter (LES)
8. RELATIONS OF THORACIC PART:-
ANTERIOR RELATIONS:- Trachea.
1. Trachia
2. Left recurrent laryngeal nerve.
3. Left principal bronchus.
4. Pericardium.
5. Left atrium
POSTERIOR RELATIONS:-
1. Bodies of the thoracic vertebrae.
2. Thoracic duct.
3. Azygos vein.
4. Right posterior intercostal arteries.
5. Descending thoracic aorta (at the lower end).
9. LATERAL RELATIONS
On the Right side:
1. Right mediastinal pleura.
2. Terminal part of the azygos vein.
On the Left side:
1. Left mediastinal pleura.
2. Left subclavian artery.
3. Aortic arch.
4. Thoracic duct
10. The esophagus has 3 areas of narrowing:
Superiorly: level of cricoid cartilage,
juncture with pharynx
Middle: crossed by aorta
and left main bronchus
Inferiorly: diaphragmatic sphincter
They have a considerable clinical importance:
1. They may cause difficulties in passing an
esophagoscope or gastroscope.
2. In case of swallowing of caustic liquids this
is where the burning is the worst and strictures develop.
3. The esophageal strictures are a common
site of esophageal carcinoma.
12. Anatomy- innervation
The innervation of the
oesophagus comprises:-
An extrinsic Parasympathetic
and sympathetic supply and
the intrinsic intramural
plexuses.
Parasympathetic Supply
provides the predominant
motor and sensory innervation
of the oesophagus.
14. LYMPH DRAINAGE
The upper third is drained in the deep cervical
nodes.
The middle third is drained into the superior and
inferior mediastinal nodes.
The lower third is drained in the celiac lymph nodes
in the abdomen.
15. Esophageal physiology
1. Fasting State:- the oesophageal body is relaxed
and the upper and lower oesophageal sphincters are
tonically contracted to prevent gastro-oesophageal
reflux and aspiration.
2. Swallowing state:-
The oropharyngeal phase : Swallowing begins when
a food bolus is propelled into the pharynx from the
mouth. It is voluntary.
16. The esophageal phase. It is involuntary.
It takes approximately 8 to 10 seconds from initiation of
the swallow to entry into the stomach .
In rapid sequence and with precise coordination, the
larynx is elevated and the epiglottis seals the airway.
17. Primary Peristalsis:
Food bolus, contracts
proximally to distally
Secondary Peristalsis:
Esophageal distention(residual
food bolus)and reflux
Tertiary Contractions:
Nonperistaltic propel bolus in a
retrograde direction to
proximal esophagus
18. Esophageal Symptom Assessment
Heartburn.
Dysphagia:sensation of food being delayed in its
normal passage from mouth to stomach. Patients often
complain of a sensation of food “sticking.”
Odynophagia.
Regurgitation.
Aspiration.
21. Esophageal testing:- endoscopy
Endoscopic Evaluation. The first diagnostic test in
patients with suspected esophageal disease is usually
upper gastrointestinal endoscopy.
Evaluation:- Mucosa Structural abnormalities.
Rigid or flexible, the flexible fiberoptic esophagoscope
is the instrument of choice because of its technical
ease, patient acceptance, and the ability to
simultaneously assess the stomach and duodenum.
Diagnostic and/or therapeutic
22. Esophageal testing endoscopy :
indications
Weight loss
Upper gastrointestinal bleeding,
Dysphagia, odynophagia and chest pain,
Partial or no response to empiric therapy,
Evaluation for Barrett's esophagus
Foreign body
23. Complication of reflux disease High Grade dysplasia in Barrett’s
mucosa,
Early adenocarcinoma arising in
Barrett’s mucosa.
24. Esophageal testing:- radiography
Radiographic Evaluation:- Barium swallow evaluation is
undertaken selectively to assess anatomy and motility.
The anatomy of large hiatal hernias are more clearly
demonstated by contrast radiology than endoscopy,
and the presence of coordinated esophageal peristalsis
can be determined by observing several individual
swallows of barium traversing the entire length of the
organ, with the patient in the horizontal position.
25. Esophageal disorders shown clearly by a full-column
technique include:-
circumferential carcinomas,
peptic strictures,
large esophageal ulcers,
and hiatal hernias.
26. Esophageal testing manometry
Measures:-
Intraluminal pressures .
Coordination of the pressure activities of LES,
esophageal body, and UES.
Assessment of patients with symptoms suggestive of
esophageal motor dysfunction ( achalasia ,
Scleroderma,DES )
27. Twenty-four-hour pH and combined
pH impedance recording
Prolonged measurement of pH is now accepted as the
most accurate method for the diagnosis of gastro-
oesophageal reflux.
It is particularly useful in patients with atypical reflux
symptoms, those without endoscopic oesophagitis and
when patients respond poorly to intensive medical
therapy.
28. Prolonged monitoring of esophageal pH is performed
by placing the pH probe or telemetry capsule 5 cm
above the manometrically measured upper border of
the distal sphincter for 24 hours.
It measures the actual time the esophageal mucosa is
exposed to gastric juice, measures the ability of the
esophagus to clear refluxed acid, and correlates
esophageal acid exposure with the patient’s symptoms.
30. Oesophageal Tears
Oesophageal tears are ruptures to any part of
oesophageal wall. Although rare, full ruptures have a
mortality of between 50 – 80%, so early recognition
and treatment is essential.
There is a wide spectrum in the severity of
oesophageal tears, the main two subcategories being
superficial mucosal tears (Mallory-Weiss tears) and
full thickness ruptures(perforation).
31. Oesophageal Perforation
Oesophageal perforation is a full thickness
rupture of the oesophageal wall; if it is spontaneous
(often due to vomiting), it is often called Boerhaave’s
syndrome.
Perforation will result in leakage of stomach contents
into the mediastinum and pleural cavity, which
triggers a severe inflammatory response which
will rapidly become overwhelming, resulting in a
physiological collapse, multi-organ failure, and death.
Rapid identification and management is therefore
essential.
32. Oesophageal rupture is a surgical emergency and
patients deteriorate rapidly, rapid identification and
management is therefore essential.
Etiology
The two most common causes are iatrogenic (such as
endoscopy) or after severe forceful vomiting.
The most common site of perforation is just above the
diaphragm in the left postero-lateral position, although
it can occur elsewhere in the oesophagus.
They are rare, with an incidence of 3.1 per million per
year and most cases occur in patients with an
otherwise normal oesophagus.
33. Clinical Features
The classic picture* is of a patient who presents
with severe sudden-onset
retrosternal chest pain,
respiratory distress,
and subcutaneous emphysema following severe
vomiting or retching.
34. Investigation
Routine bloods, including a group and save, must be
taken urgently for all those with suspected perforation.
Initial imaging via a chest radiograph (CXR) may
demonstrate evidence of
pneumomediastinum or intra-thoracic air-fluid
levels (however do not delay definitive imaging while
awaiting the CXR)
The investigation of choice is an urgent CT chest
abdomen pelvis with IV and oral contrast
35. Management
These patients are often septic and
haemodynamically unstable. Urgent and
aggressive resuscitation is therefore essential.
Definitive management varies depending on whether
the perforation was spontaneous or iatrogenic and on
the age and comorbidity of the patient.
36. The principles of definitive management (both
operative and non-operative) following initial
resuscitation involves
Control of the oesophageal leak
Eradication of mediastinal and pleural contamination
Decompress the oesophagus (typically via a trans-
gastric drain or endoscopically-placed NG tube)
Nutritional support
37. Surgical Management
The majority of patients with a spontaneous perforation
will need immediate surgery to control the leak and wash
out of the chest. This is almost always via
a thoracotomy.
Patients also need an on-table endoscopy to determine
the site of perforation and therefore the site of the incision.
Leakage is common and the patients should have a CT
scan with contrast at 10-14 days before starting oral
intake. They may therefore warrant a feeding
jejunostomy to be inserted at the time of surgery for
nutrition
38. Non-Operative Management
Patients with iatrogenic perforations are often more
stable than those with spontaneous perforations* and
may be suitable for non-operative management.
Other patients potentially suitable for non-operative
management include those with minimal
contamination, a contained perforation, no symptoms
or signs of mediastinitis, or no solid food in pleura or
mediastinum
39. Non-operative treatment involves:
Initial suitable resuscitation and transfer to Intensive
Care / High Dependency Unit
Appropriate antibiotic and anti-fungal cover
Nil by mouth for 1-2 weeks, with endoscopic insertion
of an NG tube on drainage
Large-bore chest drain insertion
Total Parenteral Nutrition (TPN) or feeding jejunostomy
insertion
40. Prognosis
Morbidity and mortality is high (between 50–80%)
and therefore early identification and treatment will
most influence outcomes.
41. Mallory-Weiss Tears
Mallory-Weiss tears are lacerations in the
oesophageal mucosa, usually at the gastro-
oesophageal junction.
They tends to occur after a period of profuse
vomiting, and in turn results in a short period of
haematemesis. They account for approximately 5% of
all cases of haematemesis.
They are generally small and self-limiting, in the
absence of clotting abnormalities or anti-coagulation
drugs. Presentation with haemorrhagic shock is
possible but rare.
42.
43. Investigation and Management
The investigation and management of Mallory-Weiss
tears is the same as for any other upper GI bleed.
Most cases can be managed conservatively, rarely
warranting interventional or surgical management.
45. GASTRO-OESOPHAGEAL
REFLUX DISEASE
Gastro-oesophageal reflux disease (GORD) is a
condition whereby gastric acid from the stomach leaks
up into the oesophagus.
It is a very common problem, affecting around a quarter
of the population in Western countries and represents
approximately 4% of primary care appointments. It
is twice as common in men compared to women.
46. pathophysiology
The lower oesophageal sphincter controls the
passage of contents from the oesophagus to the
stomach.
As part of its normal function, episodic sphincter
relaxation is expected, yet in GORD these episodes
become more frequent and allow the reflux of
gastric contents into the oesophagus.
The refluxed acidic gastric contents (or rarely alkaline
bile) result in pain and mucosal damage in the
oesophagus
47. Risk Factors
The risk factors for gastro-oesophageal reflux disease
include :-
age
obesity
male gender
alcohol
smoking
caffeinated drinks, and fatty or spicy foods.
48. Clinical features
The classic triad of symptoms is retrosternal burning
pain (heartburn), epigastric pain (sometimes radiating
through to the back) and regurgitation.
Most patients do not experience all three.
Symptoms are often provoked by food, particularly
those that delay gastric emptying (e.g. fats, spicy
foods).
As the condition becomes more severe, gastric juice
may reflux to the mouth and produce an unpleasant
taste, often described as ‘acid’ or ‘bitter’.
49.
50. The Los Angeles Classification of
Reflux
The Los Angeles classification can be used to grade
reflux oesophagitis based on severity from the
endoscopic findings of mucosal breaks in the distal
oesophagus:
Grade A – breaks ≤5mm
Grade B – breaks >5mm
Grade C – breaks extending between the tops of ≥2
mucosal folds, but<75% of circumference
Grade D – circumferential breaks (≥75%)
51. Relationship Between Hiatal Hernia
and Gastroesophageal Reflux
Disease.
A hiatal hernia can occur from long-lasting GERD or
GERD could be a symptom of a hiatal hernia.
When GERD progresses, it can cause the lower
esophageal sphincter to lose its function, which may
cause a hiatal hernia.
A hiatal hernia could also worsen GERD symptoms.
52. A hiatal hernia occurs when the hole in the diaphragm
(hiatus) through which food and liquids pass from the
esophagus into the stomach enlarges. This facilitates
acid reflux and can cause the stomach to slide upward
into the chest.
This condition in severe cases can lead to more
serious complications such as obstruction or
strangulation of the stomach.
53.
54. Investigations
GERD is a clinical diagnosis & many patients can
be treated without investigations:-
Endoscopy. to confirm the presence of esophagitis.
24 hour intra luminal pH monitoring of the esophagus.
Esophageal manometry.
Barium study: It may show a hiatus hernia.
55. Differential Diagnosis
Important gastrointestinal differentials to consider
include:
Malignancy (oesophageal or gastric)
Peptic ulceration
Oesophageal motility disorders
Oesophagitis
56. Management
All patients with gastro-oesophageal reflux
disease should be advised to take conservative
steps in its management, including avoiding known
precipitants (alcohol, coffee, fatty foods), weight loss,
and smoking cessation.
Medical Management
Proton pump inhibitors (in addition to lifestyle
changes) are the first-line treatment and are very
effective for the majority of patients.
57. Surgical Therapy for
Gastroesophageal Reflux Disease
Indications for an antireflux operation include the
following :
Failure of medical management
Complications of GERD (eg, Barrett esophagitis or
peptic stricture)
Patient preference (eg, desire to discontinue medical
therapy because of quality-of-life concerns, financial
concerns, or inability to tolerate medication)
58. Extraesophageal manifestations (asthma, hoarseness,
cough, chest pain, aspiration)
Mixed and paraesophageal hernia
Recurrent reflux or complications after previous
antireflux surgical therapy
59. Nissen Fundoplication
The Most common surgical procedure is the
NissenFundoplication.
NIssen fundoplication is the definitive surgical
treatment for GERD.
During the Nissen fundoplication, the upper part of the
stomach is wrapped around the LES to strengthen the
sphincter, prevent acid reflux, and repair a hiatal
hernia.
60.
61. Complications of GORD
Stricture
Reflux-induced strictures occur mainly in late middle-
aged and elderly people, but they may present in
children.
Esophageal stricture are generally smooth , scarred
,circumferential narrowing usually in the distal
esophagus, These can cause food to become “stuck”
or can cause pain when swallowing (Odynophagia,
Dysphagia) and treated with per-endoscopic dilatation.
62. Barrett’s oesophagus (columnarlined
lower oesophagus)
Barrett’s oesophagus is a metaplastic change in the
lining mucosa of the oesophagus in response to
chronic gastro-oesophageal reflux.
The hallmark of ‘specialised’ Barrett’s epithelium is the
presence of mucus-secreting goblet cells (intestinal
metaplasia).
It may be difficult to distinguish a Barrett’s oesophagus
from a tubular, sliding hiatus hernia during endoscopy,
as the two often coexist
65. GIANT DIAPHRAGMATIC (HIATAL)
HERNIAS
A hernia is defined as the protrusion of a whole or
part of an organ through the wall of the cavity that
contains it into an abnormal position.
A hiatus hernia describes the protrusion of an
organ from the abdominal cavity into the thorax
through the oesophageal hiatus. This is typically the
stomach herniating although rarely small bowel, colon,
or mesentery can also herniate through*.
66. Hiatus hernia are extremely common, however the
exact prevalence in the general population is difficult to
accurately state, simply because the majority are
completely asymptomatic.
However it is estimated that around a third of
individuals over the age of 50 have a hiatus hernia.
67. Classification
Hiatus herniae can be classified into two subtypes:-
Sliding hiatus hernia (80%)– the gastro-oesophageal
junction (GOJ), the abdominal part of the oesophagus,
and frequently the cardia of the stomach move or
‘slides’ upwards through the diaphragmatic hiatus into
the thorax.
68. Rolling or Para-Oesophageal hernia (20%) – an
upward movement of the gastric fundus occurs to lie
alongside a normally positioned GOJ, which creates a
‘bubble’ of stomach in the thorax. This is a true hernia
with a peritoneal sac.
The proportion of the stomach that herniates is variable and
may increase with time, eventually may evolve to
have almost the entire stomach sitting in the thorax.
A mixed type hiatus can also occur, which has both a
rolling and sliding component.
70. Incidence and Etiology
Structural deterioration of the phrenoesophageal
membrane over time may explain the higher incidence
of hiatal hernias in the older age group.
These changes involve thinning of the upper fascial
layer of the phrenoesophageal membrane (i.e., the
supradiaphragmatic continuation of the endothoracic
fascia) and loss of elasticity in the lower fascial layer
(i.e., the infradiaphragmatic continuation of the
transversalis fascia).
71. Risk Factors
Age is the biggest risk factor for developing a hiatus
hernia, due to a combination of age-related loss of
diaphragmatic tone, increasing intrabdominal pressures
(e.g. repetitive coughing), and an increased size of
diaphragmatic hiatus.
Pregnancy, obesity, and ascites are also risk factors,
due to increased intra-abdominal pressure and superior
displacement of the viscera.
72. Clinical Features
The vast majority of hiatus herniae are
completely asymptomatic.
Patients may experience gastroesophageal reflux
symptoms, such as burning epigastric pain, which is
made worse by lying flat and are often more severe
and treatment-resistant.
Other signs and symptoms that can occur
include vomiting and weight loss(a rare but serious
presentation)
73. bleeding and / or anaemia (secondary to oesophageal
ulceration).
hiccups or palpitations (if the hiatus hernia is of
sufficient size, it may cause irritation to either the
diaphragm or the pericardial sac),
swallowing difficulties (either oesophageal stricture
formation or rarely incarceration of the hernia).
The clinical examination is typically normal. In
patients with a sufficiently large hiatus hernia, bowel
sounds may be auscultated within the chest.
74. Differential Diagnosis
The important differentials that must be thought of and
excluded are:
Cardiac chest pain
Gastric or pancreatic cancer*
Particularly if there is evidence of gastric outlet obstruction,
early satiety, or weight loss.
Gastro-oesophageal reflux disease
75. Investigations
Oesophagogastroduodenoscopy (OGD) is the gold
standard investigation, (showing upward displacement
of the Gastro-Oesophageal Junction (GOJ, also termed
the ‘Z-line’).
They can also be diagnosed incidentally, either on a
CT or MRI scan*. A contrast swallow may also be used
to diagnose a hiatus hernia, although are less
commonly used
76. Figure – An OGD of a Hiatus Hernia, showing upward displacement of the Z-line
77. Management
Conservative
The first line pharmacological management for a
symptomatic hiatus hernia is a Proton Pump
Inhibitor (PPIs).
Any patient should be advised of lifestyle modification,
including weight loss, alteration of diet (low fat,
earlier meals, smaller portions).
Smoking cessation and reduction in alcohol
intake should be advised,
78. Surgical Management
Surgical management is indicated when:
Remaining symptomatic, despite maximal medical
therapy
Increased risk of strangulation/volvulus* (rolling type
or mixed type hernia, or containing other abdominal
viscera)
Nutritional failure (due to gastric outlet obstruction)
79. There are two aspects of hiatus
hernia surgery:
Cruroplasty – The hernia is reduced from the
thorax into the abdomen and the hiatus reapproximated
to the appropriate size. Any large defects usually
require mesh to strengthen the repair.
Fundoplication – The gastric fundus is wrapped
around the lower oesophagus and stitched in place
(Fig. 4)
Aims to strengthen the LOS thus helping to prevent reflux
and keep the GOJ in place below the diaphragm – the wrap
may be full or partial (usually dependent on surgeon
preference)
80. Complications of Surgery
Despite complications, the success rate of repair is
excellent with some centres reporting that >90% of
patients have a good long term outcome. The specific
complications relating to hiatus hernia surgery may
include:
Recurrence of the hernia
Abdominal bloating
Dysphagia
Fundal necrosis
81. Complications
Hiatus hernias, especially the rolling type, are prone
to incarceration and strangulation, like any other
type of hernia.
A gastric volvulus can also occur whereby the
stomach twists on itself by 180 degrees, leading to
obstruction of the gastric passage and tissue necrosis,
and requires prompt surgical intervention.
Clinically, this can present with Borchardt’s triad:
Severe epigastric pain
Retching without vomiting
Inability to pass an NG tube
82. ESOPHAGEAL DIVERTICULA
An esophageal diverticulumi s an outpouching of
mucosa through the muscular layer of the
esophagus
It can be asymptomatic or cause dysphagia and
regurgitation.
Diagnosis is made by barium swallow; surgery is rarely
required.
There are several types of esophageal diverticula, each
of different origin.
83. Diverticula of the esophagusmay be characterized by
their location in the esophagus(proximal, mid-, or distal
esophagus), or by the nature of concomitant pathology.
Diverticula associated with motor disorders are termed
Pulsion diverticula and those associated with
inflammatory conditions are termed Traction
Diverticula.
84. Classification
1.According to the origin:
a)congenital;
b)acquired.
2. According to the histological structure:
a)true (have all layers of esophageal wall);
b)false (absent muscular layer of esophageal wall).
85. 3. According to the localization:
a)pharyngoesophageal(Zenker's);
b)bifurcational;
c)epiphrenic.
4. According to the clinical course:
a)complicated;
b)uncomplicated.
86. Zenker's(pharyngeal) diverticula
Zenker's(pharyngeal) diverticula are posterior
outpouchings of mucosa and submucosa through the
cricopharyngeal muscle, probably resulting from an
incoordination between pharyngeal propulsion and
cricopharyngeal relaxation.
The most common esophageal diverticulum
Occurs between the ages of 30-50 (believed to be
acquired)
87.
88. KEY POINTS: FOUR SYMPTOMS OF ZENKER'S
DIVERTICULUM
Regurgitation of undigested food
Bad breath (Halitosis)
Lump on side of neck
Dysphagia in lower neck
“gurgling” sound when drinking
Complications:
Malnutrition : results from patient being unable to eat
well
Aspiration pneumonia
89. Midesophageal(Traction) Diverticula
Are typically associated with
mediastinalgranulomatousdisease (TB, histoplasmosis)
or secondarily, by motility disorders.
They are usually small with a blunt tapered tip that
points upward
These are usually an incidental finding on barium
swallow
90. Epiphrenic(Supradiaphragmatic)
Diverticula
Generally occur within the distal 10cm of the thoracic
esophagus
These are pulsiondiverticulathat arise due to
esophageal motor dysfunction or mechanical distal
obstruction (hiatalhernia, DES, achalasia, reflux
esophagitisand carcinoma)
91. Diffuse intramural esophageal
diverticulosis
Diffuse intramural esophageal diverticulosisis due to
dilation of the deep esophageal glands and may lead to
chronic candidiasis or to the development of a stricture
that is usually high up in the esophagus.
These patients may present with dysphagia.
92. Symptoms and Signs
Traction and epiphrenicdiverticulaare rarely
symptomatic, although their underlying cause may be.
Diagnosis and Treatment
All diverticulaare diagnosed by videotaped barium
swallow. Specific treatment is usually not required,
although resection is occasionally necessary for large
or symptomatic diverticula(removed by surgically –
cricopharyngeal myotomy).
Diverticula associated with motility disorders require
treatment of the primary disorder (distal myotomy).
94. Oesophageal motility disorders
The esophagus functions solely to deliver food from the
mouth to the stomach where the process of digestion
can begin.
Efficient transport by the esophagus requires a
coordinated, sequential motility pattern that propels
food from above and clears acid and bile reflux from
below.
Disruption of this highly integrated muscular motion
limits delivery of food and fluid, as well as causes a
bothersome sense of dysphagia and chest pain.
95. Primary esophageal causes of dysmotility include
Achalasia
Diffuse esophageal spasm
Eosinophilic esophagitis
Systemic disorders causing esophageal dysmotility
include
Systemic sclerosis
Chagas disease
96. Achalasia
Achalasia is a neurogenic esophageal motility disorder
characterized by impaired esophageal peristalsis and a
lack of lower esophageal sphincter relaxation during
swallowing.
Achalasia is thought to be caused by a loss of ganglion
cells in the myenteric plexus of the esophagus,
resulting in denervation of esophageal muscle.
97. Etiology of the denervation is unknown, but viral and
autoimmune causes are suspected, and certain tumors
may cause achalasia either by direct obstruction or as
a paraneoplastic process.
Chagas disease which causes destruction of
autonomic ganglia, may result in achalasia.
Increased pressure at the lower esophageal sphincter
(LES) causes obstruction with secondary dilation of the
esophagus.
Esophageal retention of undigested food and liquid is
common.
98. clinical presentations:
solid dysphagia 90-100% (75% also with dysphagia to
liquids)
post-prandial regurgitation 60-90%
chest pain 33-50%
pyrosis 25-45%
weight loss
nocturnal cough and recurrent aspiration
99. Investigations
1. Chest x ray showing: Absence of gases in the
fundus of the stomach.
2. Barium swallow: Dilated esophagus, the lower end
gradually narrows (bird's beak deformity).
3. Upper endoscopy: For diagnosis & to exclude
cancer esophagus, in achalasia the endoscope can
pass easily through the narrowing without resistance.
4. Manometry: It shows aperistalsis with failure of the
lower esophageal sphincter to relax
100. Figure -The characteristic feature of achalasia on barium swallow; a bird’s beak appearance caused
by failure of relaxation of the lower oesophageal sphincter
101. Treatment
Balloon dilation or surgical myotomy of the LES
Peroral endoscopic myotomy
Sometimes botulinum toxin injection
No therapy restores peristalsis; treatment of achalasia
is aimed at reducing the pressure at the LES.
102. Pneumatic Dilation
Pneumatic dilation is an endoscopic therapy for
achalasia.
An air-filled cylinder-shaped balloon disrupts the
muscle fibers of the lower esophageal sphincter, which
is too tight in patients with achalasia.
103. How is Pneumatic Dilation
Performed?
During an outpatient upper endoscopy, the endoscopist
passes a catheter with a deflated balloon through the
mouth and into the stomach.
The balloon is centered over the lower esophageal
sphincter and inflated with air.
The pneumatic dilating balloon used to treat achalasia
is 30 to 40 mm (about 1.2 to 1.6 inches) in diameter.
If symptoms do not improve adequately with the first
dilation, a second or third procedure may be performed
at a later date with a larger dilator.
104. Pneumatic dilation is often performed with X-ray
guidance.
Perforation is the major complication, The risk of
perforation increases with bigger balloons, and they
should be used cautiously for progressive dilatation
over a period of weeks.
Forceful dilatation is curative in 75–85% of cases.
105. Laparoscopic HELLER’S MYOTOMY
Laparoscopic Heller myotomy has now become the
method most commonly used to treat achalasia.
The goal of treatment is to relieve the functional outflow
obstruction secondary to the loss of relaxation.
At the time of laparoscopy, the muscle fibers of the
esophagus are teased apart to reduce the LES
pressure.
Advantages of this method are the shorter length of
stay (1 day), minimal postoperative discomfort, and
excellent response rate of 90%
106. The major complication is gastro- oesophageal reflux,
and most surgeons therefore add a partial anterior
fundoplication (Heller–Dor operation).
107. Peroral Endoscopic Myotomy
(POEM)
Peroral endoscopic myotomy (POEM) is an endoscopic
therapy for achalasia.
It uses upper endoscopy rather than conventional
surgery, which involves an incision in the skin. In
patients with achalasia, the lower esophageal sphincter
is too tight.
The goal of all treatment of achalasia is to weaken the
lower esophageal sphincter
108. How Is POEM Performed?
While the patient is under general anesthesia, the
endoscopist passes the flexible endoscope through the
mouth into the esophagus.
A small incision is made in the innermost layer of the
esophagus (the mucosa). The endoscope is then
tunneled down the remaining length of the esophagus
in the layer called the submucosa.
In the lower esophagus, the endoscopist cuts the
muscle fibers of the lower esophageal sphincter.
The endoscope is removed and the first incision made
in the mucosa is closed to complete the procedure.
109. Diffuse Oesophageal Spasm
Diffuse oesophageal spasm (DOS) is a disease
characterised by multi-focal high amplitude
contractions of the oesophagus.
It is thought to be caused by the dysfunction of
oesophageal inhibitory nerves. In some individuals,
DOS can progress to achalasia.
110. Clinical Features
Patients with diffuse oesophageal spasm will typically
present with severe dysphagia to both solids and
liquids. Central chest pain is a common finding,
usually exacerbated by food.
Interestingly, the pain from DOS can respond to
nitrates, making it difficult to distinguish from angina
pectoris (yet this pain is rarely exertional). Examination
is often normal.
111. Investigations
Diffuse oesophageal spasm is investigated in the same
manner as other motility disorders, with the definitive
diagnosis made via manometry.
Endoscopy is usually normal.
Manometry characteristically shows a pattern
of repetitive, simultaneous, and ineffective
contractions of the oesophagus. There may also be
dysfunction of the lower oesophageal sphincter.
112. Figure 4 – Barium swallow showing a corkscrew appearance, as seen in cases of diffuse
oesophageal spasm
113. Management
The initial management is through agents which act to
relax the oesophageal smooth muscle,
typically nitrates or calcium channel blockers (CCBs) as
first line. These limit the strongest of the contractions, and
so provide a symptomatic improvement, although their
long-term efficacy is uncertain.
Patients with diffuse oesophageal spasm and documented
hypertension of the lower oesophageal sphincter may
benefit from pneumatic dilatation.
Myotomy is reserved for the most severe cases and must
be used with caution
114. Other Causes of Oesophageal
Dysmotility
A number of autoimmune and connective tissue
disorders are associated with oesophageal
dysmotility. These include systemic sclerosis (most
common), polymyositis, and dermatomyositis.
In these cases treatment is directed at the underlying
cause (e.g. immunosupression in autoimmune-
mediated disease), with nutritional
modification and proton pump inhibitors as
required.
116. CARCINOMA OF THE ESOPHAGUS
More than 8,500 new cases of oesophageal
cancer are diagnosed each year, with the incidence of
cancers of the lower oesophagus / gastro-oesophageal
junction rinsing faster than any other solid organ
tumour. They are 3 times more common in men.
There are two main types of oesophageal cancer:
Squamous cell carcinoma (more common in the
developing world) typically occurring in the middle and
upper thirds of the oesophagus
Strongly associated with smoking and excessive alcohol
consumption, as well as chronic achalasia, low vitamin A
levels and, rarely, iron deficiency
117. Adenocarcinoma (more common in the developed
world) typically occurring in the lower third of the
oesophagus
Arises as a consequence of metaplastic epithelium (termed
Barrett’s oesophagus) which progresses to dysplasia, to
eventually become malignant
Risk factors for this subtype are long-standing GORD,
obesity, and high dietary fat intake
Other rare subtypes of esophageal malignancy include
leiomyosarcoma, rhabdomyosarcoma, or lymphoma.
118. Clinical Features
Early stage oesophageal cancer often lacks well-
defined symptoms, which may account for the majority
of patients presenting in the later course of the disease.
However, as the condition progresses, the symptoms
that can present include:
Dysphagia – characteristically progressive, initially
being to solids (especially meats or breads) then liquids
Any patient with dysphagia should be assumed to have
oesophageal cancer until proven otherwise.
119. Significant weight loss – due to both dysphagia and
cancer-related anorexia (this is a marker of late-stage
disease)
Other less common symptoms include odonyphagia or
hoarseness
120. NICE guidance states the red-flag symptoms for a
suspected oesophageal malignancy requiring urgent
endoscopy are:
Patients with dysphagia
Any patient >55yrs with weight loss and upper
abdominal pain, dyspepsia, or reflux
On clinical examination, patients may have evidence of
recent weight loss or cachexia, signs of dehydration,
supraclavicular lymphadenopathy, or any signs of
metastatic disease (e.g. jaundice, hepatomegaly, or
ascites)
121. Differential Diagnosis
Importantly, the dysphagia should be classified as
either a mechanical or neuromuscular disorder, as this
can significantly affect future investigations.
However, any patient presenting with dysphagia should
be assumed to have oesophageal cancer until proven
otherwise.
122.
123. Investigations
Initial Investigations
Any patient with a suspected oesophageal malignancy
should be offered urgent upper
gastrointestinal endoscopy* (also termed an
oesophago-gastro-duodenoscopy, OGD), to be
performed within 2 weeks.
Any malignancy seen on OGD will be biopsied and
sent for histology.
*Patients who are not fit for an OGD can occasionally
have a CT scan (neck and thorax) however this is
much less sensitive and specific.
125. Further Investigations
Before undergoing curative treatment, patients often
require a variety of the staging investigations including:
CT Chest-Abdomen-Pelvis and PET-CT scan are
used together to investigate for distant metastases
Endoscopic Ultrasound to measure the penetration
into the oesophageal wall (T stage) and assess and
biopsy suspicious mediastinal lymph nodes
Staging laparoscopy (for junctional tumours with an
intra-abdominal component) to look for intra-peritoneal
metastases
126. Any palpable cervical lymph nodes may be investigated
via Fine Needle Aspiration (FNA) biopsy and any
hoarseness or haemoptysis may warrant investigation
via bronchoscopy.
127. Management
Sadly, the majority of patients present with advanced
disease. Approximately 70% of patients are therefore
only treated palliatively.
As with all cancers, the management of oesophageal
cancer patients should be determined by
the multidisciplinary team (MDT), with input from
general surgeons, oncologists, specialist nurses,
nutritionists, and the palliative care team.
128. Curative Management
The choice of curative treatment strategy will
depend on tumour type, site and the patient’s general
fitness and co-morbidities.
For the majority of patients, this comprises surgery with
or without neoadjuvant chemotherapy or chemo-
radiotherapy (CRT):
129. Squamous cell carcinomasSCCs of the upper
oesophagus are technically difficult to operate on and
definitive CRT is therefore usually the treatment of
choice
SCCs of the middle or lower oesophagus will warrant
either definitive CRT or neoadjuvant CRT followed then
by surgery
130. Adenocarcinomas– neoadjuvant chemotherapy or
chemo-radiotherapy followed by an oesophageal
resectionPatients who are less fit (but still fit enough to
undergo surgery) may simply receive surgical
treatment alone
131. Surgical Treatment
Surgical treatment is a major undertaking as both the
abdominal and chest cavities need to be opened.
Patients have one lung deflated for about 2 hours
during surgery; 30-day mortality rates are around 4%
and it takes 6-9 months for patients to recover to their
pre-operative quality of life.
The main complications are anastomotic leak*
(8%), re-operation, pneumonia (30%), and death (4%)
132. Post-operative nutrition is a major problem for these
patients as they lose the reservoir function of the
stomach. Many centres will routinely insert a feeding
tube into the small bowel (a “feeding jejunostomy”) to
aid nutrition.
However, most patients will need to eat 5-6 small
meals per day and “graze” to meet their nutritional
requirements as they physically cannot fit in 3 normal
size but intermittent meals.
133. Surgical Techniques
The main surgical management option for oesophageal
cancer is an oesophagectomy, with a variety of
approaches possible. They all involve removal of the
tumour, top of the stomach, and surrounding lymph
nodes. The stomach is then made into a tube (“the
conduit”) and brought up into the chest to replace the
oesophagus.
134. Specific approaches include:
Right thoracotomy with laparotomy (termed an Ivor-
Lewis procedure)
Right thoracotomy with abdominal incision and neck
incision (termed a McKeown procedure)
Left thoracotomy with or without neck incision
Left thoraco-abdominal incision (one large incision
starting above the umbilicus and extending round the
back to below the left shoulder blade)
135. For a small number of patients with very early cancers
or high grade Barrett’s oesophagus, an option is
Endoscopic Mucosal Resection (EMR), which is the
removal of just the mucosal layer of the oesophagus.
EMR can be combined with radiofrequency ablation
(RFA) or photodynamic therapy (PDT) afterwards to
destroy any malignant cells that may be left.
136. Palliative Management
Those patients deemed too unfit or unsuitable for
curative therapy can be offered a range of palliative
options.
Patients with difficulty in swallowing should have
an oesophageal stent placed where possible (Fig.
3). Radiotherapy and/or chemotherapy can be used
for palliation to reduce tumour size and bleeding,
temporarily improving the patient’s symptoms.
Photodynamic therapy (PDT) is a treatment that uses
a photosensitizing agent, that when exposed to a
specific wavelength of light produces a form of oxygen
that kills nearby cells.
137. Nutritional support is essential for this patient group,
as progression of the disease can lead to significant
dysphagia and cachexia. Thickened
fluid and nutritional supplements should be offered
(usually via the nutrition team).
If dysphagia becomes too severe to tolerate enteral
feeds, a Radiologically-Inserted Gastrostomy (RIG)
tube may need to be inserted, to bypass the
obstruction.
138.
139. Prognosis
The prognosis for oesophageal cancer is generally
poor due to late presentation. Overall five-year survival
is 5-10%.
The outcome of surgically treated patients have
survival depending on stage of the disease, with a 5
year survival for stage 1 cancers at around 60%.
Palliative treated patients have a median survival of 4
months.
