Dysphagia

Dysphagia is an important problem in surgical patients. I have discussed Introduction, Zenker's diverticulum, GERD, Achalasia Cardia and Carcinoma Esophagus. If you watch all these videos together, i assure you that you will become confident in managing a case of dysphagia.

1. DYSPHAGIA
INTRODUCTION
AN OVRVIEW
Dr.B.SelvarajMS;Mch;FICS;
Professor of Surgery
Melaka Manipal Medical college
Melaka 75150 Malaysia

2. Must To Know Core Clinical
Problems
1.Acute RLQ pain
2.Acute RUQ pain
3.Acute epigastric pain
4.Acute LLQ pain
5.Dysphagia 6.Abdominal lumps 7.Upper GI hemorrhage
8.Lower GI hemorrhage
9.Obstructive Jaundice
10.Breast lumps, Mastalgia & Nipple
discharge
11.Neck swellings- Thyroid
& Non thyroidal
12.Groin swellings
13.Scrotal swellings
14.Limb ischemia- Acute & Chronic
15.Varicose veins, DVT & Pulmonary Embolism
16.Renal & ureteric colic
17.Hematuria
18.Acute retention of urine

3. DYSPHAGIA
Surgical Anatomy
Physiology of deglutition/swallowing
Causes of Dysphagia
History/ Symptoms
Physical Examinations/ Signs
Investigations
Diagnostic Algorithm

4. ANATOMY

5. PHYSIOLOGY OF DEGLUTITION
1.Oral Phase: (Buccal) Voluntary Food moistened with saliva
Tongue pushes food bolus backward
2.Pharyngeal Phase: Stimulation of tactile receptors in oropharynx
and initiation of swallow reflex
Tongue blocks oral cavity
Soft palate blocks nasopharynx
Larynx moves up & vocal folds closes
Epiglottis covers larynx
Respiration temporarily suspended
Upper esophageal sphincter opens to allow
food bolus
3.Esophageal phase: Involuntary Esophageal peristalsis
Larynx moves down

6. DYSPHAGIA-CAUSES

7. Difficulty In Swallowing
Dysphagia:
Difficulty in swallowing
;
High dysphagia
(oro-pharyngeal and upper
esophageal) describe difficulty in initiating a swa llow;
Low dysphagia
(lower
oesophageal) feel the food getting stuck a few seco nds after swallowing
.
Odynophagia:
painful swallowing due to carcinoma or candidiasis
Globus
:
the common sensation of having a lump in the throat without true
dysphagia. Globus is very common and its etiology is poorly understood –
however, only a small proportion of affected patien ts will seek medical help and it
is an entirely benign condition
May be

8. DYSPHAGIA
What is the duration of the
symptoms?
Days to weeksCa Esophagus
Months to yearsMotility disorders
Is the dysphagia progressive or
intermittent?
Progressive dysphagiamechanical
obstruction like stricture (benign or
malignant)
Intermittent dysphagiafunctional
obstruction like motility disorders.
History/Symptoms
Is the dysphagia to solids, fluids, or
both?:
If patient is able to swallow fluids but
unable to swallow solids to begin
withprobably it is mechanical
obstruction like stricture(benign or
malignant)
In late stages, in mechanical
obstruction there is dysphagia for
solids and liquids
If dysphagia is more for fluids over
solidsmotility disorders like
Achalasia
cardia
What questions would you like to ask specifically about the swallowing?

9. DYSPHAGIA
Is there any coughing? Coughing immediately after
swallowingStroke/ Parkinson’s
disease- oropharyngeal incoordination
Coughing sometime after meals
GERD and Pharyngeal pouch
Is there any choking? Functional problem with the
oropharyngeal phase of swallowing.
Is there any gurgling or heartburn? GurglingPharyngeal pouch
Heartburn- PyrosisGERD
History/Symptoms
Weight loss & Nocturnal cough: Weight lossCa Esophagus or any
severe dysphagia
Nocturnal cough: GERDAspiration
Neurological symptoms (In functional dysphagia), like early
dysphagia for liquids
Rheumatological symptoms CREST syndrome:
Calcinosis
Raynaud’s
Esophageal dysmotility
Sclerodactyly & Telangiectasia.
Any associated symptoms?

10. DYSPHAGIA
1. Cranial nerve pathology: Important if the history suggests
functional dysphagia like bulbar palsy
2. Signs of GI malignancy: Patients cachectic and Virchow’s node
palpableCarcinoma Esophagus
Palpable epigastric massCarcinoma
esophagus extending to cardia
3. Koilonychia: Iron-deficiency anemia which can cause
Plummer–Vinson syndrome.
Physical Exam/Signs
4. Neck mass: In Pharyngeal pouch on left side neck
Huge goiter compress trachea and
cause dysphagia
5. Features of CREST syndrome: Calcinosis
Raynaud’s
Esophageal dysmotility
Sclerodactyly
Telangiectasia
What are the relevant aspects of the physical examination?
There is relatively little that can be gained from the examination of a patient
with dysphagia, but there are five features that ar e particularly relevant:

11. DYSPHAGIA
1. Barium Swallow: A cineradiographic study which
monitors the passage of a bolus of
barium contrast medium from the upper
to the lower esophageal sphincter of a
supine patient.
Barium swallow is useful in
investigating patients who may have a
high lesion and achalasia cardia.
2. Videofluroscopy: Modified form of barium swallow in
which upright patients are given
barium.
3. 24 Hrs PH monitoring:
In GERD
INVESTIGATIONS
3. Upper GI Endoscopy: Allows visualization of luminal and
mural lesions, as well as the
opportunity to biopsy and treat lesions
Various procedures, such as stricture
dilatation, stent insertion, laser
coagulation, and Botox injections can
be done
4. Manometry: Assesses the pressures in the LES and
the peristaltic wave in the rest of the
esophagus
Manometry is the key investigation for
diagnosing a motility disorder.

12. DYSPHAGIA
Diagnostic Algorithm

13. Peripheral Arterial Diseases(PAD)

14. ZENKER’S DIVERTICULUM
DYSPHAGIA
AN OVRVIEW
Dr.B.SelvarajMS;Mch;FICS;
Professor of Surgery
Melaka Manipal Medical college
Melaka 75150 Malaysia

15. ZENKER’S DIVERTICULUM
Causes for Dysphagia
Etiopathogenesis
Clinical features
Investigations
Treatment
Treatment Algorithm
Mindmap

16. DYSPHAGIA-CAUSES

17. ZENKER’S DIVERTICULUM
Etiopathogenesis
A pulsion diverticulum of the mucosa and submucosa of the esophagus, just above the
cricopharyngeal muscle (i.e. above the upper esophageal shincter) which is not relaxing.
Most common esophageal diverticulum due to loss of coordination in second stage of swallowing
resulting in increased luminal pressure.
Mainly affects elderly males. It has an incidence of 2 per 100,000 per year in the UK

18. ZENKER’S DIVERTICULUM
Clinical Features
Progressive cervical dysphagia
and sense of a lump in the throat.
Food might get trapped in the outpouching, leading to:
-
Regurgitation
, reappearance of ingested food in the mouth.
-
Cough,
due to food regurgitated into the airway. Aspiratio n &
Pneumonia rare
-
Halitosis
, smelly breath, as stagnant food is digested by
microorganisms
-
Infection
of diverticulum
It rarely, if ever, causes any pain.
Cervical webs
are seen associated in 50% of patients with this
condition
Usually there is
H/O loss of weight
A
left-sided neck mass.

19. ZENKER’S DIVERTICULUM
INVESTIGATIONS
Barium Swallow:
- Reveal the diverticulum
- A cineradiographic study which
monitors the passage of a bolus of
barium contrast medium from the
upper to the lower esophageal
sphincter of a supine patient.
Barium Videofluroscopy:
-Modified form of barium swallow
in which upright patients are given
barium

20. ZENKER’S DIVERTICULUM
UPPER GI ENDOSCOPY
Upper GI Endoscopy:
- Should be done only if the
esophagogramrevealed some doubtful
growth in the diverticulum
- Otherwise normally we need not do
upper GI endoscopy for fear of
perforating the esophagus

21. ZENKER’S DIVERTICULUM
TREATMENT
Treatment involves surgery because there
is no effective medical therapy
Open Surgery
:
Diverticulectomy with
Cricopharyngeal myotomy
or
Diverticulopexy
is performed through a
Lt neck incision for large diverticulum.
If diverticulum is <2cms only Myotomy
Endoscopic myotomy-
An operating
laryngoscope is used to expose the neck of
the diverticulum, and a myotomy is
performed using an endoscopic linear
stapler.
With this technique , the diverticulum
becomes part of a common channel with
the cervical esophagus-
“Dohlman’s
procedure”.

22. DYSPHAGIA
Diagnostic Algorithm

23. ZENKER’S DIVERTICULUM
Treatment
Algorithm

24. ZENKER’S DIVERTICULUM
MIND MAP

25. Peripheral Arterial Diseases(PAD)

26. GASTRO ESOPHAGEAL
REFLUX DISEASE
(GERD)
DYSPHAGIA
AN OVRVIEW
Dr.B.Selvaraj
MS;Mch;FICS;
“Surgical Educator”
Malaysia

27. GASTRO-ESOPHAGEAL
REFLUX DISEASE Causes of dysphagia
Definition
Etiology
Pathophysiology
Clinical Features-Symptoms & Signs
Complications
Investigations-Workup
Management
Mindmap
Diagnostic algorithm
Treatment algorithm

28. DYSPHAGIA-CAUSES

29. GERD
DEFINITION
Montreal consensus panel (44 experts):
“Retrograde flow of stomach contents into esophagus
causing troublesome symptoms and/or complications”
Troublesome—patient has to decide when reflux
interferes with lifestyle

30. GERD
Why do we care about reflux?
Patients experience reflux symptoms
• 44% monthly
• 20% weekly
• 4-7% daily
Most common gastrointestinal diagnosis on outpatient physician
visits
Frequency and severity does not predict esophagitis, stricture, or
cancer development

31. GERD
GE JUNCTION-ANATOMY

32. GERD
ANTI REFLUX MECHANISMS
EsophagealSphincter Tone and Length.
Sling Fibres of the Cardia.
EsophagealHiatus Tone.
Positive Intra Abdominal Pressure.
Gastroesophageal acute angle of His
Esophagealmucosal rosette

33. GERD
LOWER ESOPHAGEAL SPHINCTER
Normally, the lower esophagealsphincter exists as a zone of high
pressure between esophagusand stomach; when the HPZ is lost,
reflux occurs
Three components of high pressure zone
Resting pressure if <8mmHg
Overall length if < 3cms
Intra-abdominal length if < 1cm Reflux occurs

34. GERD
ETIOLOGY
Sliding Hiatus Hernia.
Alteration of Phreno-esophagealLigament.
Altered Obliquity of GE junction.
Reduced pinching action of Crus of Diaphragm
Reduced LES Pressure.
Altered Transient Relaxation period in LES -TLESR

35. GERD
ETIOLOGY

36. GERD
PATHOPHYSIOLOGY
Fundicdistention (overeating) & delayed
gastric emptying (high fat)
Lower esophagealsphincter is pulled distally
by expanding fundus
Squamous epithelium exposed to gastric juice.
Repeated exposure columnisation
Extension of inflammation into muscularis
propriacauses progressive loss in length and
pressure of the LES—“esophagealshortening”
Loss of LES leads to regurgitation, heartburn,
and subsequent severe esophagitis

37. GERD
PATHOPHYSIOLOGY

Spectrum of disease theory:
Nonerosivediseaseerosive diseaseBarrett’sesophageal
adenocarcinoma

38. GERD
CLINICAL FEATURES
Heartburn-Pyrosis
Retrosternal pain1-2 hours after
eating, often at night, relieved
by antacids
Regurgitation (Waterbrash)
Spontaneous return of gastric
contents proximal to GE jxn
into mouth; less well relieved
with antacids
Dysphagia (40%)—difficulty
with swallowing should prompt
search for pathologic condition
Stricture esophagus
Hoarseness of Voice /
Dysphonia
Respiratory Symptoms
Cough / Expectoration
Wheeze / Breathlessness
Aspiration

39. GERD
COMPLICATIONS
Peptic Ulceration
Hemetemesis
Stricture Esophagus
Barrett’s esophagus
Adeno Carcinoma esophagus
Laryngeal Complications
-Hoarseness of voice
-Dysphonia
Respiratory Complications
-Cough / Expectoration
-Wheeze / Breathlessness
-Aspiration

40. GERD
INVESTIGATIONS
Upper G.I. Endoscopy
Upper G.I. Contrast Studies
24 Hours Ambulatory pH Monitoring
EsophagealManometry

41. GERD
UPPER GI ENDOSCOPY
Grade A
Grade B
Grade C&D

42. GERD
BARRETT’S ESOPHAGUS
Intestinal / Gastric Columnar Metaplasia of the
distal esophagus from squamous to columnar
epithelium
Diagnosed on Upper G.I.Endoscopy.
Pre Malignant condition, leads
to Adeno Carcinoma.
Multiple Biopsies are required
to exclude Malignancy.

43. GERD
HIATUS HERNIA

44. GERD
HIATUS HERNIA

45. GERD
HIATUS HERNIA
Only 40% of patients with classic
symptoms of GERD will have reflux
observed on radiography
Assess for:
•Esophageal shortening
•Hiatal hernia (80%)
•Paraesophageal hernia
•Stricture or obstructing lesion
•Beading or corkscrewing (motility
disorders)
Sliding
Hiatus Hernia
Para-esophageal
Hiatus Hernia

46. GERD
AMBULATORY 24 Hrs
pH MONITORING
Rationale: gold standard
for diagnosis of GERD
Quantifies actual time the
esophageal mucosa is exposed to
gastric juice
Measures the ability of the esophagus to clear
refluxed acid
Correlates esophageal acid exposure
with patients symptoms
Without abnormal pH study, surgery is
unlikely to benefit
Gives a composite score (Johnson- DeMeester
score) highly sensitive and specific (>96%) for
diagnosing GERD

47. GERD
AMBULATORY 24 HrspH Monitoring

48. GERD
ESOPHAGEAL MANOMETRY
Quantifies
esophagel
peristalsis
Rules out
esophageal
motility
disorders

49. GERD
TREATMENT
Treatment Goals for GERD
Eliminate symptoms
Heal esophagitis
Manage or prevent complications
Maintain remission

50. GERD
TREATMENT
Lifestyle Modifications are Cornerstone of GERD Therapy
Elevate head of bed 4-6 inches
Avoid eating within 2-3 hours of bedtime
Lose weight if overweight
Stop smoking
Modify diet
Eat more frequent but smaller meals
Avoid fatty/fried food, peppermint, chocolate,
alcohol, carbonated beverages, coffee and tea
OTC medications prn

51. GERD
MEDICAL TREATMENT

52. GERD
ENDOSCOPIC TREATMENT
To date, there have been basically three approaches to endo-luminal treatment
for GERD:
Radiofrequency energy ablation
delivered to the lower oesophageal
sphincter (LES);
Endoscopic gastroplasty plication of
the gastric folds immediately distal to
the oesophago-gastric junction;
Endoscopic implantation of a bulking
agent or polymer in the region of the
LES.
Tiny magnetic beads
act as an artificial
sphincter preventing
acid reflux.
Strettais a minimally
invasive endoscopic
procedure, RFQ energy
produce thickening of
LES

53. GERD
SURGICAL TREATMENT
Indications
Need for continuous drug treatment
or escalating dose of PPI
Relatively young
Financial burden or noncompliance
with PPI
Patient choice
Factors predictive of successful outcome
following antireflux surgery (n = 199)
-Abnormal score on 24-hour
esophageal pH monitoring (p <0.001
-Presence of typical symptoms
of GERD
(heartburn and regurgitation) (p< 0.001)
- Symptomatic improvement in
response to acid suppressive
therapy (p = 0.02)

54. GERD
SURGICAL TREATMENT
Principles of surgery
Establish effective LES pressure
Position the LES within the abdomen
-Sphincter is under positive (intra-
abdominal) pressure
Close any associated hiatal defect
Key points of surgery
Complete dissection of esophageal
hiatus and both crura
Mobilization of the gastric fundus
Closure of the associated hiatal defect
Creation of a tensionless gastric wrap
around esophagus
50- to 60-French intraesophageal
dilator
Limiting the length of the wrap to 1.5
to 2.0 cm
Stabilizing the wrap

55. GERD
Lap Nissen’sFundoplication
TOUPET
FUNDOPLICATION

56. GERD MIND MAP

57. DYSPHAGIA
Diagnostic Algorithm

58. GERD
Treatment Algorithm

59. Peripheral Arterial Diseases(PAD)

60. ACHALASIA CARDIA
DYSPHAGIA
AN OVRVIEW
Dr.B.Selvaraj
MS;Mch;FICS;
“Surgical Educator”
Malaysia

61. ACHALASIA CARDIA
Objectives
Causes for dysphagia
Etiopathogenesis of achalasia
Clinical features of achalasia
Workup of achalasia
Management of achalasia
New development in the treatment of
achalasia
Mindmap
Diagnostic Algorithm
Treatment Algorithm

62. DYSPHAGIA-CAUSES

63. ACHALASIA CARDIA
History of Achalasia Cardia
In 1913 Ernest Heller performed the
first surgical intervention for achalasia
and the procedure still bears his name
It was not actually called achalasia
until a 1927 article by Arthur Hurst
-The treatment of achalasia of the
cardia: so-called ‘cardiospasm’
-Achalasia is Greek for lack of
relaxation
Ellis et al described the first
transthoracic approach in 1958
The first laparoscopic Heller myotomy
by Prof Sir Alfred Cuschieri in 1991

64. ACHALASIA CARDIA
ETIOLOGY
Failure of the lower portion of the esophagus to relax during
swallowing is defined as achalasia. The resulting dysphagia
is due to three mechanisms:
1. Complete absence of peristalsis in the esophageal body.
2. Incomplete/impaired relaxation of the LES after
swallowing.
3. Increased resting tone of the LES.
Idiopathic
Decreased number of ganglion cells in myenteric Auerbach’s
plexus
Chagasic, which is caused by Chagas disease, a parasitic
infection of the esophageal musculature by Trypanosoma
cruzi
Pseudoachalasia , which is caused by extrinsic compression
of the lower esophagus by masses (e.g. , tumors, hematoma,
and enlarged lymph nodes)
Achalasia (Greek ‘failure to relax’)

65. ACHALASIA CARDIA
PATHOLOGY
Histologic examination shows a decrease in the neurons of the myenteric
plexuses (Auerbach’s plexus)
There is a preferential decrease in the nitric oxid e producing cells which
contribute to LES relaxation
There is a relative sparing of the cholinergic neur ons responsible for maintaining
LES tone
The loss of these inhibitory neurons leads to an in creased resting tone in the LES
It also leads to aperistalsis of the esophagus
These result in elevation of intraluminal esophageal pressure, esophageal
dilatation, and subsequent progressive loss of normal swallowing mechanisms—
a functional holdup of ingested material.

66. ACHALASIA CARDIA
Clinical Features
Dysphagia:
-Most common symptom of achalasia is dysphagia
-Patients often report that food sticks in their ch est
-Liquids to begin with and then for solids also
-They tend to augment the passage of food by drinking liquids
Regurgitation:
-Because of functional obstruction
-The passive return of food to the mouth after eati ng.
Loss of weight: in 60% of patients
Chest pain: occurs in 43% of those with achalasia. Heartburn & Halitosis
may occur as retained food and liquids in the dista l esophagus ferment.
Pulmonary complications: include cough and chronic aspiration. They occur
in 10% to 30% of those with achalasia

67. ACHALASIA CARDIA
INVESTIGATIONS
Onset of symptoms is slow and gradual. The average time between
onset of symptoms and diagnosis is over four years.
In patients with suspected achalasia, there are thr ee important
tools in diagnosing achalasia
1.Barium swallow
2.Upper GI Endoscopy
3.Esophageal Manometry

68. ACHALASIA CARDIA
BARIUM SWALLOW
Classic features include esophageal
dilatation,loss of peristalsis, delayed
emptying with a column of barium
retained within the esophagus, smooth
tapering to a classic
“Bird’s Beak”appearance
Uniform dilation of the esophagus is
known as “ Sigmoid esophagus” or
" Cucumber esophagus"

69. ACHALASIA CARDIA
UPPER GI ENDOSCOPY
All patients with suspected
achalasia should undergo
endoscopy to rule out malignancy
On entering the esophagus, it is
usually large and will potentially
have retained food
While the LES does not open
spontaneously, it can be passed
with gentle pressure.
Closed or tight LES on passage of
the endoscope into the stomach.

70. ACHALASIA CARDIA
ESOPHAGEAL MANOMETRY
Manometry of the esophagus is the
gold standard for diagnosing achalasia.
Classic findings include:
1. Aperistalsis of the smooth muscle
segment of the esophagus, where the
contractile pressures are usually low.
2. Elevated resting LES pressure (often
above 45 mmHg)
3. Abnormal relaxation of the LES:
- The LES should drop to <8 mmHg
- In achalasia LES relaxation in
response to a swallow may be
incomplete or absent.

71. ACHALASIA CARDIA
TREATMENT
Treatment is directed to relieve the symptoms, not to relieve the pathology

72. ACHALASIA CARDIA
TREATMENT
Medical therapy
Nitratesgiven sublingually can
decrease LES pressure and offer
short-term relief of dysphagic
symptoms. However, they do not
affect LES function, and efficacy
decreases over time
Calcium-channel blockers can
decrease LES pressure and relieve
dysphagic symptoms. However, as
with nitrates, the function of the LES
does not improve, side effects are
common, and efficacy is short-lived.
Botulinumtoxin A
Botulinumtoxin blocks release of
acetylcholine at nerve receptors
and,when injected into the LES, leads
to relaxation of the LES by inhibiting
the function of the unopposed neurons
that cause LES contraction.
Three-fourths of patients respond to an
initial inj ection
Efficacy decreases over time with
multiple treatments and recurrence
after 6 months.

73. ACHALASIA CARDIA
TREATMENT
Compared to botulinumtoxin and medications, pneumatic dilatation is the
most effective nonsurgical therapy.
Involves passing the pneumatic device to the LES, using both endoscopy and
fluoroscopy to properly place the balloon
The balloon is inflated to a pressure between 7 to 15 psi
Pneumatic dilatation forcefully disrupts the hypertrophied muscle fibers of the
LES, leading to decreased LES pressure
Patients are usually observed for six hours and then discharged home
Complications include a 1% to 6% risk of esophagealperforation
Endoscopic graded pneumatic dilatation

74. ACHALASIA CARDIA
TREATMENT
Endoscopic graded Pneumatic dilatation BOTOX- BotulinumInjection

75. ACHALASIA CARDIA
TREATMENT
Heller’s Cardiomyotomy
The operation consists of splitting the longitudina l muscle fibers and dividing
the circular muscle fibers of the distal esophagus at the area of the LES.
The myotomy is carried down onto the gastric cardia for 2 to 3 cms,
The operation can be performed through the chest or abdomen and is most
commonly done via laparoscopy
A fundoplication is usually performed along with the myotomy because 30% to
40% of patients develop symptomatic gastroesophageal reflux disease (GERD).
Anterior Dor or posterior 270* Toupet fundoplication is done
Myotomy lowers LES pressure more reliably than medication, botulinumtoxin,
or pneumatic dilatation

76. ACHALASIA CARDIA
TREATMENT
Heller’s Cardiomyotomy
Anterior Dorfundoplication
Posterior 270* Toupet fundoplication

77. ACHALASIA CARDIA
NEW TREATMENT
POEM- Per Oral Endoscopic Myotomy
The leading expert in this technique is
Dr.Haruhiro Inoue, from Showa University
Northern Yokohama Hospital in Japan
Uses an endoscope with a special transparent
cap
Start by entering the submucosal space
approximately 15 cm above the GE junction.
Using a solution of saline with indigo dye, a
tunneled dissection is carried distally to about
2 cms past the GE junction
Then, myotomy is begun starting 10 cm
proximal to GE junction
Myotomy is carried distally down to 2 cm
past the GE junction
Myotomy only takes the inner circular fibers
while leaving the outer longitudinal fibers
intact.
At the end of the procedure, the scope is
removed from the submucosal tunnel and the
entry site is closed with endoscopic clips
Dr. Haruhiro Inoue

78. ACHALASIA CARDIA
NEW TREATMENT
POEM- Per Oral Endoscopic Myotomy

79. ACHALASIA CARDIA
MIND MAP

80. DYSPHAGIA
Diagnostic Algorithm

81. ACHALASIA CARDIA
Treatment Algorithm

82. Peripheral Arterial Diseases(PAD)

83. CARCINOMA OF ESOPHAGUS
DYSPHAGIA
AN OVRVIEW
Dr.B.Selvaraj
MS;Mch;FICS;
“Surgical Educator”
Malaysia

84. CARCINOMA OF ESOPHAGUS
Causes for Dysphagia
Etiology
Pathology
Clinical features
Investigations
Treatment
Complications
Mindmap
Diagnostic Algorithm for dysphagia
Treatment Algorithm

85. DYSPHAGIA-CAUSES

86. CARCINOMA OF ESOPHAGUS
Is the 6th most common malignancy Incidence:
General: 20 per 100 000; Age: 50 - 70 ; Whites : blac ks = 1 : 5
Sites:
Upper 1/3rd: 17%; Middle 1/3rd: 50%; Lower 1/3rd: 33%
Types:

87. CARCINOMA OF ESOPHAGUS
ETIOLOGY
#Autosomal dominant disorder characterized
hyperkeratosis of palms, soles & leucoplakia
##Characterized by dysphagia, Fe-deficiency
anemia, glossitis, cheilosis & esophageal webs
*These are risk factors for 1squamous cell Ca &
2adenoCa

88. CARCINOMA OF ESOPHAGUS
PATHOLOGY

Histological type:
squamous carcinoma (upper
two-thirds of oesophagus); adenocarcinoma
(middle third, lower third and junctional).

Worldwide squamous carcinoma is commonest
(80%) but adenocarcinoma accounts for >50%
in USA and UK.
Spread:
lymphatics, direct extension, vascular
invasion
Direct extension:
- longitudinally along the wall
- Laterally through the wall into adjacent
structures- trachea, lungs & aorta
Lymphatic:
direction of spread to regional
lymphatics is predominantly caudal
- Any regional lymph node from the superior
mediastinum to the coeliac axis and lesser curve
of the stomach may be involved.
Vascular:
involve liver, lungs, brain and
bones.
Tumours arising from the intra-abdominal
portion of the esophagus may also
disseminate
transperitoneally
.

89. CARCINOMA OF ESOPHAGUS
CLINICAL FEATURES
Clinical findings suggestive of
advanced malignancy include
recurrent laryngeal nerve palsy,
Horner’s syndrome,chronic spinal
pain.
Surgical cure unlikely include
weight loss of more than 20%
Palpable lymphadenopathy in the
neck is a sign of advanced disease

90. CARCINOMA OF ESOPHAGUS
INVESTIGATIONS
Upper GI Endoscopy and Biopsy
Barium Swallow
Endoscopic Ultrasound
CECT- contrast Enhanced CT
Bronchoscopy
PET- Scan
MRI- Scan

91. CARCINOMA OF ESOPHAGUS
UPPER GI ENDOSCOPY
Gold standard investigation
Can determine
a) Location
b) Nature (friable/ firm/ polypoidal)
c) Proximal & distal extent
d) Relationship to cricopharyngeus,
cardia
Squamous cell
carcinoma
Adeno Carcinoma
In chromoendoscopy,
Lugol’s Iodine & Toluidine
Blue are used (NORMAL
tissues take up dye)

92. CARCINOMA OF ESOPHAGUS
BARIUM SWALLOW
Recommended for all patients with
dysphagia
Differentiates between…
a) intrinsic mass (protrudes into lumen)
b) extrinsic mass (compression by
structures outside esophagus)
Classical findings: apple core lesion,
shouldering sign (near-horizontal
upper border of Ba+shadow), rat tail
appearance
Can also demonstrate tracheo-
esophageal fistula
Apple Core
Shouldering
&
Rat tail
Tracheo-
esophageal
fistula

93. CARCINOMA OF ESOPHAGUS
BARIUM SWALLOW

94. CARCINOMA OF ESOPHAGUS ENDOSCOPIC ULTRASOUND
Gold standard for staging any GI
tumor
Determines
1. Tumor depth
2. Status of regional lymph nodes-
can also take biopsy
3. However can not differentiate T1 &
T2 lesions preciously

95. CARCINOMA OF ESOPHAGUS
CECT
Scans needed for Thorax and Upper Abdomen.
Stage Loco-regional as well as Metastatic
Disease.
Can stage advanced stenotic lesions where
EUS is not possible.
Limitation:
-Tissue diagnosis not achieved
Can determine
- tumor length
- thickness of esophagus & stomach
- regional nodes status
- T4 lesions invading surrounding structures
- Metastasis to lungs and liver

96. CARCINOMA OF ESOPHAGUS
BRONCHOSCOPY
To assess invasion of Tracheo-
Bronchial tree
To assess vocal cord paralysis due to
infiltration of Recurrent Laryngeal N.

97. CARCINOMA OF ESOPHAGUS
PET SCAN
Not very useful for definitive staging
(hence, done ONLY after locally-
advanced lesion with no metastases
are noted in CECT)
Helps evaluate 1° mass, regional nodes
& distant disease

98. CARCINOMA OF ESOPHAGUS
MRI SCAN
Not routinely performed
Helps identify
a) T4 lesions
b) involvement of vascular, liver, neural
tissues

99. CARCINOMA OF ESOPHAGUS
TNM STAGING

100. CARCINOMA OF ESOPHAGUS
TNM STAGING

101. CARCINOMA OF ESOPHAGUS
TREATMENT
Curative( Stage I, II, III)
Stage I (T1a/N0/M0)
– Endoscopic Mucosal
Resection
Stage I and IIA disease (T1/N0/M0 – T2/N0/M0)
–
Surgical resection is potentially curative only if
lymph nodes are not involved and clear tumours
margins can be achieved
Stage IIB and III (T1/N1/M0 - T4/anyN/M0)
–
Surgery or neoadjuvant chemotherapy (cisplatin
and fluorouracil) or chemoradiation followed by
surgery or definitive chemoradiation
The role of
neoadjuvant or adjuvant chemotherapy
or
chemoradiotherapy
continues to be explored in
clinical trials.
Chemoradiotherapy and radiotherapy
are
occasionally used
with curative intent
in patients
deemed not suitable for surgery
Palliation (Stage IV disease – anyT/anyN/M1
)
Partially covered
self-expanding metal stents
are the
intubation of choice for obstructive symptoms –
especially useful when tracheo-oesophageal fistula
present ± laser therapy.
Radiotherapy
– external beam DXT or endoluminal
brachytherapy
Laser resection (Nd : YAG laser)
of the tumour to
create lumen
Photodynamic therapy:
photosensitizing agents
(given IV) are taken up by dysplastic malignant
tissue which is damaged when photons (light) is
applied.
Reconstruction is by
jejunal or gastric ‘pull-up’
or rarely colon interposition

102. CARCINOMA OF ESOPHAGUS
TREATMENT
Three surgical approaches for esophageal cancer
Transhiatal esophagectomyvia abdominal and cervical incisions
Ivor Lewis esophagectomyvia abdominal and thoracic incisions (for upper
and middle 1/3 cancers)
McKeown(also known as three-hole) esophagectomyvia abdominal, thoracic,
and neck incisions.

103. CARCINOMA OF ESOPHAGUS
TREATMENT
Transhiatal esophagectomyvia abdominal and cervical incisions
Developed to ↓ morbidity from respiratory
failure a/w transthoracic esophageal resections
Usually done for lower 1/3rd tumors
Procedure:
2 incisions made (on left neck & abdomen)
Mobilization of esophagus is done blindly with
manual manipulation thru widened hiatus
Stomach is tubularized & gently passed thru
posterior mediastinum
Cervical esophagogastric anastomosis
Accesible nodes in neck, lower chest & abdomen
are removed
Pyloroplasty + feeding jejunostomy

104. CARCINOMA OF ESOPHAGUS
TREATMENT
Ivor Lewis esophagectomyvia abdominal and thoracic incisions (for middle
and lower 1/3 cancers)
Is a combined laparotomy & right
thoracotomy
Usually done for middle 1/3rd tumors
Gastric & esophageal mobilization
Esophageal division 5 cm from gross
obvious tumor
En bloc dissection of thoracic duct, azygos
vein, ipsilateral pleura, mediastinal &
peritracheal nodes
4) Intrathoracic esophagogastric
anastomosis

105. CARCINOMA OF ESOPHAGUS
TREATMENT
McKeown(also known as three-hole) esophagectomyvia abdominal, thoracic,
and neck incisions.
Usually done for upper 1/3rd tumors
(for better longitudinal clearance)
Right thoracotomy (to mobilize thoracic
esophagus) + lymphadenectomy
Abdomen & neck incisions (for
mobilization of esophageal substitute
& placing anastomosis in neck)
Lengthy procedure
Pulmonary complications

106. CARCINOMA OF ESOPHAGUS
PALLIATIVE TREATMENT
Aims of therapy:
-To reestablish swallowing.
-To stabilize body weight. Laser therapy:
-Improve dysphagia by necrosis of tumour.
-Nd-YAG laser is commonly used. Photodynamic therapy:
-Dihematoporphyrin ether followed by
argon laser. Intubation
long lasting palliation after
single procedure.
Beneficial in 1. infiltrating stenotic or long
tumour. 2. obstruction is due to external
compression. 3. Sealing of TEF.
Tube types
Atkinson,Celestin, Souttar
Self Expanding Metallic Stents- SEMS

107. CARCINOMA OF ESOPHAGUS
COMPLICATIONS OF SURGERY
PulmonaryEmpyema&Sepsis
Anastomotic LeakMediastinitis
Conduit Necrosis
Anastomotic stricture.
Recurrent laryngeal nerve injury
Chylothorax
Gastro-esophageal reflux.
Colonic dysmotility.
Recurrence

108. CARCINOMA OF ESOPHAGUS
PROGNOSIS

109. CARCINOMA OF ESOPHAGUS
MINDMAP

110. DYSPHAGIA
Diagnostic Algorithm

111. DYSPHAGIA
Treatment Algorithm

112. Peripheral Arterial Diseases(PAD)