Download - Benging oesophageal disease surgery
Benign Esophageal Diseases
1
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
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
Clinical features Achalasia is also known to be a premalignant condition
8% chance of developing carcinoma over a 20-year period
Most commonly squamous cell carcinoma
4
Symptomsthe 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
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
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
Diagnosis Esophageal manometry is the gold
standard:i. aperistalsis of the distal esophageal bodyii. Esophageal body with pressure above
baselineiii. Low amplitude waveformsiv. incomplete or absent LES relaxationv. 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
Treatment All are palliative and do not
address the problem of decreased motility
10
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
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
Bougie dilationMay offer months of relief but
requires repeated dilations
14
Bougie dilation15
Pneumatic Dilation pneumatic dilation remains one of the
most effective first-line therapies Effective in 60% of cases Esophageal perforation 4%
16
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
19
Surgical TherapyEsophagectomy is considered in any symptomatic patient with
•tortuous esophagus (megaesophagus),
•failure of more than one myotomy
•undilatable stricture.
20
21
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
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
DiagnosisThe classic manometry findings in DES are
simultaneous multipeaked contractions of high amplitude (>120 mm Hg) or long duration (>2.5 seconds;
27
28
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
Treatment Eliminating trigger foods or drinks
from diet Peppertmint may provide
temporary reliefe Nitrates, CCB and anticholinergic
drungs?
30
31
Nutcracker esophagus The most common esophageal
hyper motility disorder Most painful of al esophageal
hypermotility disorders High amplitude peristaltic
contractions (hypertensive peristalsis)
32
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
Treatment Patients with nutcracker esophagus may have
triggers and are counseled to avoid
caffeine, cold, and hot foods.
Calcium channel blockers, nitrates,
34
35
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
Esophageal Diverticula false diverticula occur because of
elevated intraluminal pressures generated from abnormal motility disorders
37
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
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
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
41
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
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
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
45
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
47
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
49
50
51
52
53
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
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
Histological findings• Columnar epithelial gastric surface
cells
• intestinal goblet cells,
• intestinal absorptive cells with a rudimentary brush border
56
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
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
!!!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
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
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
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
64
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
66
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
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
TreatmentStudies have demonstrated regression of metaplasia to normal mucosa up to 57% of the time in patients who have undergone antireflux surgery
69
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
71
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
73
74
Caustic Injury the best cure for this condition is
prevention
75
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
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
78
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 esophagus
79
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
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
Symptoms and Diagnosis Pain in the back perforation of the
mediastinal esophagus abdominal pain abdominal visceral
perforation Hematemesis/respiratory distress severe
injury
82
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
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
85
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
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
Management of complicationsIf 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
92
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
94
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
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
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
History • trauma• advanced esophageal cancer• violent wretching • swallowing of a foreign body• recent instrumentation
98
Symptoms and DiagnosisSymptoms of neck, substernal,
or epigastric pain are consistently associated with esophageal perforation
Vomiting, hematemesis, or dysphagia also may accompany them
99
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
Symptoms and Diagnosis Abdominal perforations present
with epigastric pain that radiates to the back if the perforation is posterior
101
Examination On examination , patient may
present with tachypnea, tachycardia, and a low-grade fever but have no other overt signs of perforation
102
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
Laboratory
• elevated white blood cell count
• elevated salivary amylase level in the blood or pleural fluid
104
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
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
Diagnosis A surgical endoscopy needs to be
performed if the esophagram is negative or if operative intervention is planned.
107
108
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 catheter3.secured airway
109
Treatment• IV fluids • broad-spectrum antibiotics • patient is monitored in an ICU
The patient is kept NPO, and nutritional access needs are assessed
110
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
112
113
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
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
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
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
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.
If any of these is a factor, primary repair, even in the presence of a healthy tissue bed, is not recommended.
118
119
120
121
122
123
124
125
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
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
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
129
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
131
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
GASTROESOPHAGEAL REFLUX DISEASEGERD 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
134
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
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
Clinical Presentations of GERD Classic GERD
Extraesophageal/Atypical GERD
Complicated GERD
137
Clinical Presentations of GERD Classic GERD :
Substernal burning and or regurgitation
Postprandial
Aggravated by change of position
Prompt relief by antacid
138
Extraesophageal Manifestations of GERDPulmonary
AsthmaAspiration pneumoniaChronic bronchitisPulmonary fibrosis
Other Chest pain Dental erosion
ENTHoarsenessLaryngitisPharyngitisChronic coughGlobus sensationDysphoniaSinusitisSubglottic stenosisLaryngeal cancer
139
Clinical Presentations of GERD Symptoms of Complicated GERD :
Dysphagia Difficulty swallowing: food sticks or hangs up
Odynophagia Retrosternal pain with swallowing
Bleeding
140
Diagnostic Tests for GERD Barium swallow
Endoscopy
Ambulatory pH monitoring
Esophageal manometry
141
Treatment Lifestyle Modifications
Acid Suppression Therapy
Anti-Reflux Surgery
Endoscopic GERD Therapy
142
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 mealsAvoid fatty/fried food, peppermint, chocolate,
alcohol, carbonated beverages, coffee and tea
OTC medications prn
143
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
145
146
147