surgery oesophageal disease

1. Benign
Esophageal
Diseases
1

2. Achalasia
 Achalasia means“failure to relax” an
uncommon motility disorder
 It is characterized by degeneration of the
myenteric neurons that innervate LES and
esophageal bodyt
 this degeneration results in hypertension of the LES and failure of the LES to relax on pharyngeal swallowing, as well as
pressurization of the esophagus, esophageal dilation, and resultant loss of progressive peristalsis.
2

3. pathogenesis
presumed to be idiopathic or infectious neurogenic degeneration.
Yet studies suggest that other factors might be involved
•Severe emotional stress,
•trauma,
•drastic weight reduction,
•and Chagas’ disease (infection with T.cruzi)
3

4. Clinical features
 Achalasia is also known to be a premalignant condition
 8% chance ofdeveloping carcinoma over a 20-year period
 Most commonly squamous cell
carcinoma
4

5. Symptoms
the classic triad of presenting symptoms consists of
• dysphagia; begins with liquids and progresses to solids
• regurgitation; approximately 60% of patients
• weight loss; occurs In final disease
• However, heartburn, postprandial choking, and nocturnal coughing are commonly seen.
5

6. Clinical features
• retrosternal chest pain is experienced and can be severe until the LES opens,
• with progressive disease, aspiration can become lifethreatening.with complications like
• Pneumonia
• lung abscess
• bronchiectasis
6

7. Diagnosis
 Esophagogram:”Barium study”
• The classic finding is a gradual tapering at the end
of the esophagus, similar to a bird's beak
 Upper endoscopy
• is performed to evaluate the mucosa for evidence of esophagitis or cancer.
7

8. 8

9. Diagnosis
 Esophageal manometry is the gold standard:
i. aperistalsis of the distal esophageal body
ii. Esophageal body with pressure above
baseline
iii. Low amplitude waveforms
iv. incomplete or absent LES relaxation
v. hypertensive LES higher than 35mmhg
 vigorous achalasia
 normal to high amplitude esophageal body
contractions in the presence of a
nonrelaxing LES
 may represent an early stage of achalasia
9

10. Treatment
 All are palliative and do not address the
problem of decreased motility
10

11. Medical Therapy
 Nitrates effective treatment of achalasia
 headaches limit their tolerability by patients
 Calcium channel antagonists have a
better side-effect profile when compared
with nitrates
11

12. Botulinum Toxin
 injected into the LES targets the excitatory,
acetylcholine-releasing neurons that
generate LES basal muscle tone
 is easy to administer and associated with
relatively few side effects
 It is apparent that, with repeated injections,
the response rates reported are similar or
lower to that achieved with the initial injection
12

13. Bougie dilation
May offer months of relief but
requires repeated dilations
14

14. Bougie dilation
15

15. Pneumatic Dilation
pneumatic dilation remains one of the most
effectivefirst-line therapies
Effective in 60% of cases
 Esophageal perforation 4%
16

16. 17

17. Surgical Therapy
 acid exposure is a known complication of
surgical intervention for achalasia
 The current technique is a modification of
Heller myotomy laparoscopic or open
 Eliminates risk of cancer
18

18. 19

19. Surgical Therapy
Esophagectomy is considered in any symptomatic patient with
•tortuous esophagus (megaesophagus),
•failure of more than one myotomy
•undilatable stricture.
20

20. 21

21. 22

22. Diffuse Esophageal Spasm
 DES is a hypermotility disorder of the
esophagus
 The basic pathology is related to a motor
abnormality of the esophageal body that
is most notable in the lower two thirds of
the esophagus
 Witch results in repetitive simultaneous
and high amplitude contractions
 Muscular hypertrophy and degeneration of the branches of the vagus nerve in the esophagus have
been observed.
23

23. Symptoms and Diagnosis
 The clinical presentation of DES is typically
that of chest pain and dysphagia
 These symptoms may be related to eating
or exertion and may mimic angina
 Patients will complain of a squeezing
pressure in the chest that may radiate to
the jaw, arms, and upper back
24

24. Diagnosis
The classic manometry findings in DES are simultaneous multipeaked contractions of high
amplitude (>120 mm Hg) or long duration (>2.5 seconds;
27

25. 28

26. Treatment
 the mainstay of treatment for DES is
nonsurgical, and pharmacologic or
endoscopic intervention is preferred
 Surgery is reserved for patients with
recurrent incapacitating episodes of
dysphagia and chest pain who do not
respond to medical treatment
29

27. Treatment
 Eliminating trigger foods or drinks from
diet
 Peppertmint may provide temporary
reliefe
 Nitrates, CCB and anticholinergic drungs?
30

28. 31

29. Nutcracker esophagus
 The most common esophageal hyper
motility disorder
 Most painful of al esophageal
hypermotility disorders
 High amplitude peristaltic contractions
(hypertensive peristalsis)
32

30. Diagnosis
the gold standard of diagnosis is the
subjective complaint of chest pain
with simultaneous evidence of peristaltic esophageal contractions 2 standard deviations (SDs) above the
normal values on manometric tracings. Amplitudes higher than 400 mm Hg are common
 While the LES pressure and relaxation are
normal
33

31. Treatment
Patients with nutcracker esophagus may have triggers and are counseled to avoid
caffeine, cold, and hot foods.
Calcium channel blockers, nitrates,
34

32. 35

33. Esophageal Diverticula
 can occur in several places along the
esophagus
 The three most common sites of
occurrence are pharyngoesophageal
(Zenker's), parabronchial
(midesophageal), and epiphrenic
36

34. Esophageal Diverticula
 false diverticula occur because of
elevated intraluminal pressures generated
from abnormal motility disorders
37

35. Esophageal Diverticula
 Zenker's diverticulum and an epiphrenic
diverticulum fall under the category of
false diverticula.
 Traction, or true, diverticula result from
external inflammatory mediastinal lymph
nodes adhering to the esophagus
38

36. f
inflamed mediastinal lymph nodes from an infection with tuberculosis accounted for most cases
Infections with histoplasmosis and resultant fibrosing mediastinitis have now become more common.
39

37. Pharyngoesophageal (Zenker's)
Diverticulum
 is the most common esophageal diverticulum It
usually presents in older patients in the 7th decade
of life
 found herniating into Killian's triangle, between the
oblique fibers of the thyropharyngeus muscle and
the horizontal fibers of the cricopharyngeus muscle
40

38. 41

39. Symptoms and Diagnosis
 Commonly, patients complain of a
sticking in the throat.
 cough, excessive salivation, and
intermittent dysphagia often are signs of
progressive disease
 As the sac increases in size, regurgitation
of foul-smelling, undigested material is
common
42

40. Symptoms and Diagnosis
 Halitosis, voice changes, retrosternal pain,
and respiratory infections are especially
common in the elderly population
 The most serious complication from an
untreated Zenker's diverticulum is
aspiration pneumonia or lung abscess
43

41. Symptoms and Diagnosis
 Diagnosis is made by barium esophagram
 Neither esophageal manometry nor
endoscopy is needed to make a
diagnosis of Zenker's diverticulum.
44

42. 45

43. Treatment
 Surgical or endoscopic repair of a
Zenker's diverticulum is the gold standard
of treatment
 Open repair involve :
 myotomy of the proximal and distal
thyropharyngeus and cricopharyngeus
muscles
 diverticulectomy or diverticulopexy are
performed through an incision in the left neck
46

44. 47

45. Treatment
 An alternative to open surgical repair is
the endoscopic
Dohlman procedure : division of the
common wall between the esophagus
and the diverticulum using a laser or
stapler has also been successful
48

46. 49

47. 50

48. 51

49. 52

50. 53

51. Barrett's Esophagus
 Barrett's esophagus is a condition
whereby an intestinal, columnar
epithelium replaces the stratified
squamous epithelium that normally lines
the distal esophagus
 Chronic gastroesophageal reflux is the
factor that both injures the squamous
epithelium and promotes repair through
columnar metaplasia
54

52. Barrett's Esophagus
 10% of patients with GERD develop
Barrett's esophagus
 40-fold increase in risk for developing
esophageal carcinoma in patients with
Barrett's esophagus
 Prospectively following 100 patients with Barrett’s esophagus for 1 year an incidence of 1%/year for developing
adenocarcinoma, a similar risk to that of patients with a 20 pack-year smoking history developing lung cancer.
55

53. Histological findings
• Columnar epithelial gastric surface cells
• intestinal goblet cells,
• intestinal absorptive cells with a rudimentary brush border
56

54. Barrett's Esophagus
 With continued exposure to the reflux
disaese, metaplastic cells undergo
cellular transformation to low- and high-
grade dysplasia
 these dysplastic cells may evolve to
cancer
57

55. Barrett's Esophagus
 70% of patients are men aged 55 to 63
years
 Men have a 15-fold increased incidence
over women of adenocarcinoma of the
esophagus
58

56. !!!
many investigators believe that once metaplasia is present, it is exposure to bile and other reflux related
substances, not necessarily acid, that encourages the progression of dysplasia to cancer.
**In vitro studies have demonstrated cellular and molecular changes in cells of all types when exposed to bile
salts.
**it has been shown that patients with adenocarcinoma of the distal esophagus are three times more likely to
have been taking acid suppression medications
59

57. Pathophysiology
An incompetent LES, with or without a hiatal hernia, plays an important role in the
development of GERD and Barrett’s esophagus.
Factors that have been implicated in the pathophysiology of the LES
• age
• obesity
• stress
• caffeinated products
• alcohol
• tobacco
• spicy, fatty, and acidic
foods.
60

58. Symptoms and Diagnosis
 Many patients are asymptomatic
 Most patients present with symptoms of GERD.
• Heartburn
• regurgitation
• acid or bitter taste in the mouth
• excessive belching
 Recurrent respiratory infections, adult asthma, and
infections in the head and neck also are common
complaints.
62

59. Symptoms and Diagnosis
 The diagnosis of BE is made by
endoscopy and pathology
 The presence of any endoscopically
visible segment of columnar mucosa
within the esophagus that on pathology
identifies intestinal metaplasia defines BE
63

60. 64

61. Treatment
 Yearly surveillance endoscopy is
recommended in all patients with a
diagnosis of Barrett's esophagus
 For patients with low-grade dysplasia,
surveillance endoscopy is performed at 6-
month intervals for the first year and then
yearly thereafter if there has been no
change
65

62. 66

63. Treatment
 Patients undergoing surveillance are
placed on acid suppression medication
and monitored for changes in their reflux
symptoms.
 Controversy surrounds the benefits of
antireflux surgery in patients with Barrett's
esophagus
67

64. The controversy
 Surgeons: medical therapy and
endoscopic surveillance may treat the
symptoms but fail to address the problem,
the functional impairment of the LES
 gastroenterologists: adequate
surveillance for the development of
cancer is impossible after a
fundoplication
68

65. Treatment
Studies have demonstrated regression of
metaplasia to normal mucosa up to 57% of
the timein patients who have undergone
antireflux surgery
69

66. Ablative therapy
 Photodynamic therapy (PDT) is the most common
ablative method used to treat BE
• Complication:
 Esophageal strictures 34%
 Persistent metaplasia 50%
 Endoscopic mucosal resection (EMR) is gaining
favor for the treatment of Barrett's esophagus with
low-grade dysplasia.
 Increase in stricture rate with larger resictions
70

67. 71

68. Treatment
 Esophageal resection for Barrett's
esophagus is recommended only for
patients in whom high-grade dysplasia is
found
 Pathologic data on surgical specimens
demonstrate a 40% risk for
adenocarcinoma within a focus of high-
grade dysplasia
72

69. 73

70. 74

71. Caustic Injury
 the best cure for this condition is
prevention
75

72. Caustic Injury
 Alkali ingestion is more common than
acid ingestion because of its lack of
immediate symptoms
 Acids cause an immediate burning
sensation in the mouth
 alkali ingestion are much more
devastating and almost always lead to
significant destruction of the esophagus
76

73. Caustic injury
there are several sites that are prone to injury because of a relative delay in transit
through the esophagus.
They correlate to the anatomic narrowings
i. the level of the UES,
ii. midesophagus where the aorta abuts the left mainstem bronchus,
iii. proximal to the LES.
77

74. 78

75. Alkali ingestion
• Alkaline substances dissolve tissues by liquefactive necrosis, that penetrates the
tissue
• there are three phases of tissue injury from alkali ingestion
bands constrict the esopha
79

76. Acid ingestion
 Very difficult, immediate burning pain
 Causes coagulate necrosis
 Formation of eschar limits the tissue
penetration!
 Rarely causes full thickness injury
 Within 48hrs the extent of the injury is
already determind
80

77. Symptoms and Diagnosis
 During phase one, patients may complain of
 oral and substernal pain
 hypersalivation
 odynophagia
 dysphagia
 Hematemesis
 vomiting
 During stage two, these symptoms may disappear
only to see dysphagia reappear as fibrosis and
scarring begin to narrow the esophagus throughout
stage three
81

78. Symptoms and Diagnosis
 Pain in the back  perforation of the mediastinal
esophagus
 abdominal pain abdominal visceral perforation
 Hematemesis/respiratory distress  severe injury
82

79. Physical exam
 evaluating the mouth, airway, chest, and
abdomen
 Careful inspection of the lips, palate,
pharynx, and larynx is done
 signs of perforation
 Auscultation to the lungs upper airway
involvement
83

80. Endoscopy
 Early endoscopy is recommended 12 to
24 hours after ingestion
 identify the grade of the burn
 C.I
 Hemodynamic instability
 Evidence of perforation
84

81. 85

82. Treatment acute phase
 limiting and identifying the extent of the
injury
 It begins with neutralization of the
ingested substance
 Alkalis are neutralized with half-strength
vinegar or citrus juice
86

83. Treatment
 Acids are neutralized with milk, egg
whites, or antacids
 Emetics and sodium bicarbonate need to
be avoided because they can increase
the chance of perforation
87

84. Management of complications
If full-thickness perforation of the esophagus or stomach is found at any time 
•emergent exploratory laparotomy is indicated.
•esophagus and stomach and all affected surrounding organs and tissues are resected,
•end-cervical esophagostomy is performed, and a feeding jejunostomy is placed
Postoperatively, the patient is monitored in the ICU and managed aggressively.
91

85. 92

86. Late complications
 Esophageal squamous cell carcinoma
The risk for development of esophageal
squamous cell carcinoma is 1000-fold
higher in victims of alkali ingestion as
compared to the general population
93

87. 94

88. Esophageal Perforation
 Perforation of the esophagus is a surgical
emergency
 Early detection and surgical repair within
the first 24 hours results in 80% to 90%
survival
 after 24 hours, survival decreases to less
than 50%
95

89. Esophageal Perforation
 Most esophageal perforations occur after
endoscopic instrumentation for a
diagnostic or therapeutic procedure,
 Perforation from forceful vomiting
(Boerhaave's syndrome), foreign body
ingestion, or trauma accounts for 15%,
14%, and 10% of cases, respectively
 Other iatrogenics: endothracheal tube
minitracheostomy and injury during
dissections
96

90. Boerhaave’s Syndrome
Recurrent emesis disrupts the normal vomiting reflex that enables sphinchter relaxation, resulting in an increase in intrathoracic
esophageal pressure and perforation.
A tear in the esophageal mucosa, known as a Mallory-Weiss tear, also occurs after persistent retching, but is not associated with
perforation.
97

91. History
• trauma
• advanced esophageal cancer
• violent wretching
• swallowing of a foreign body
• recent instrumentation
98

92. Symptoms and Diagnosis
Symptoms of neck, substernal, or
epigastric pain are consistently
associated with esophageal
perforation
Vomiting, hematemesis, or
dysphagia also may accompany
them
99

93. Symptoms and Diagnosis
 Cervical perforations may present with
neck ache and stiffness due to
contamination of the prevertebral space
 Thoracic perforations present with
shortness of breath and retrosternal chest
pain lateralizing to the side of perforation
100

94. Symptoms and Diagnosis
 Abdominal perforations present with
epigastric pain that radiates to the back if
the perforation is posterior
101

95. Examination
 On examination , patient may present
with tachypnea, tachycardia, and a low-
grade fever but have no other overt signs
of perforation
102

96. Examination
With increased mediastinal and pleural
contamination, patients progress toward
hemodynamic instability
On exam, subcutaneous air in the neck or
chest, shallow decreased breath sounds, or
a tender abdomen are all suggestive of
perforation
Laboratory values of significance are an
elevated white blood cell count and an
elevated salivary amylase in the blood or
pleural fluid.
103

97. Laboratory
• elevated white blood cell count
• elevated salivary amylase level in the blood or pleural fluid
104

98. Diagnosis
 Diagnosis of an esophageal perforation
may be made radiographically
 A chest roentgenogram may demonstrate
a hydropneumothorax
 A contrast esophagram is done using
barium for a suspected thoracic
perforation and Gastrografin for an
abdominal perforation.
105

99. Diagnosis
 Most perforations are found above the
GEJ on the left lateral wall of the
esophagus which results in a 10% false-
negative rate in the contrast esophagram
if the patient is not placed in the lateral
decubitus position
 Chest CT shows mediastinal air and fluid
at the site of perforation
106

100. Diagnosis
 A surgical endoscopy needs to be
performed if the esophagram is negative
or if operative intervention is planned.
107

101. 108

102. Treatment
 Patients with an esophageal perforation
can progress rapidly to hemodynamic
instability and shock
 perforation is suspected, appropriate
resuscitation
1. placement of large-bore peripheral IV
catheters
2. urinary catheter
3. secured airway
109

103. Treatment
• IV fluids
• broad-spectrum antibiotics
• patient is monitored in an ICU
 The patient is kept NPO, and nutritional
access needs are assessed
110

104. Treatment
 Surgery is not indicated for every patient
with a perforation of the esophagus
 management is dependent on several
variables: stability of the patient, extent of
contamination, degree of inflammation,
underlying esophageal disease, and
location of perforation
111

105. 112

106. 113

107. Treatment
 The most critical variable that determines
the surgical management of an
esophageal perforation is the degree of
inflammation surrounding the perforation.
 When patients present within 24 hours of
perforation, inflammation is generally
minimal, and primary surgical repair is
recommended
114

108.  Clinically stable/unstable with contained
perforation  conservative therapy
• NPO and enteral access
• Endolumenal stent endoscopically placed
Partial resuloution continue conservative
therapy
Persistense/ progression surgery
115

109. Treatment
 With time, inflammation progresses, and
tissues become friable and may not be
amenable to primary repair the golden
period is within the first 24 hrs.
116

110. Surgery
• If primary repair or the muscle flap fails or if patient renders unstable, resection or
exclusion of the esophagus with a cervical esophagostomy, gastrostomy, feeding
jejunostomy, and delayed reconstruction is recommended
117

111. Surgery
 there are four underlying conditions of the esophagus that affect the treatment
1. resectable carcinoma,
2. megaesophagus from end-stage achalasia,
3. severe peptic strictures, or a
4. history of caustic ingestion.
Ifany of these is a factor, primaryrepair, even in the presence of a healthy tissue bed, is not recommended.
118

112. 119

113. 120

114. 121

115. 122

116. 123

117. 124

118. 125

119. Leiomyoma
 Leiomyomas constitute 60% of all benign
esophageal tumors
 They are found in men slightly more often
than women and tend to present in the
4th and 5th decades
 They are found in the distal two thirds of
the esophagus more than 80% of the time
126

120. Leiomyoma
 They are usually solitary and remain
intramural, causing symptoms as they
enlarge.
 Recently, they have been classified as a
gastrointestinal stromal tumor (GIST)
 GIST tumors are the most common
mesenchymal tumors of the
gastrointestinal tract and can be benign
or malignant
127

121. Symptoms and Diagnosis
 Many leiomyomas are asymptomatic
 Dysphagia and pain are the most
common symptoms and can result from
even the smallest tumors
 A chest radiograph is not usually helpful
to diagnose a leiomyoma, but on barium
esophagram, a leiomyoma has a
characteristic appearance.
128

122. 129

123. Leiomyoma
 During endoscopy, extrinsic compression
is seen, and the overlying mucosa is
noted to be intact
 Diagnosis also can be made by an
endoscopic ultrasound (EUS), which will
demonstrate a hypoechoic mass in the
submucosa or muscularis propria
130

124. 131

125. GASTROESOPHAGEAL REFLUX
DISEASE
 LES has the primary role of preventing
reflux of the gastric contents into the
esophagus
 GERD may occur when the pressure of the
high-pressure zone in the distal
esophagus is too low to prevent gastric
contents from entering the esophagus
132

126. GASTROESOPHAGEAL REFLUX DISEASE
GERD is often associated with a hiatal hernia
the most common is the type I hernia, also
called a sliding hiatal hernia
Type II and III hiatal hernias are often
referred to as paraesophageal hernias and
they may be associated with GERD
Type IV when there is other organ herniated
into the chest (Spleen ,Colon)
133

127. 134

128. GASTROESOPHAGEAL REFLUX
DISEASE
 Defintion :
 Symptoms OR mucosal damage produced
by the abnormal reflux of gastric contents
into the esophagus
 Often chronic and relapsing
 May see complications of GERD in patients
who lack typical symptoms
135

129. GASTROESOPHAGEAL REFLUX
DISEASE
 Epidemiology :
 About 44% of the US adult population have
heartburn at least once a month
 14% of Americans have symptoms weekly
 7% have symptoms daily
136

130. Clinical Presentations of
GERD
 Classic GERD
 Extraesophageal/Atypical GERD
 Complicated GERD
137

131. Clinical Presentations of
GERD
 Classic GERD :
 Substernal burning and or regurgitation
 Postprandial
 Aggravated by change of position
 Prompt relief by antacid
138

132. Extraesophageal
Manifestations of GERD
Pulmonary
Asthma
Aspiration
pneumonia
Chronic bronchitis
Pulmonary fibrosis
Other
Chest pain
Dental erosion
ENT
Hoarseness
Laryngitis
Pharyngitis
Chronic cough
Globus sensation
Dysphonia
Sinusitis
Subglottic stenosis
Laryngeal cancer
139

133. Clinical Presentations of
GERD
 Symptoms of Complicated GERD :
 Dysphagia
 Difficulty swallowing: food sticks or hangs up
 Odynophagia
 Retrosternal pain with swallowing
 Bleeding
140

134. Diagnostic Tests for GERD
 Barium swallow
 Endoscopy
 Ambulatory pH monitoring
 Esophageal manometry
141

135. Treatment
 Lifestyle Modifications
 Acid Suppression Therapy
 Anti-Reflux Surgery
 Endoscopic GERD Therapy
142

136. Treatment
 Lifestyle Modifications
 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
143

137. Anti-Reflux Surgery Indication for Surgery :
 have failed medical management
 opt for surgery despite successful medical management
(due to life style considerations including age, time or
expense of medications, etc)
 have complications of GERD (e.g. Barrett's esophagus;
grade III or IV esophagitis)
 have medical complications attributable to a large hiatal
hernia. (e.g. bleeding, dysphagia)
 have "atypical" symptoms (asthma, hoarseness, cough,
chest pain, aspiration) and reflux documented on 24
hour pH monitoring
144

138. 145

139. 146

140. 147