2. A. Esophageal perforation
B. Boerhaave & mallory weiss syndrome
C. Diffuse esophageal spasm
D. Barett esophagus
E. Achalasia
F. Zenker diverticulum
G. Plummer vinson syndrome
H. Hiatal hernia
I. Esophagitis
J. Esophageal cancer
K. Scleroderma
3. is due to the rapid increase in
intraesophageal pressure combined with
negative intrathoracic pressure caused by
vomiting.
Perforation of the esophagus can present with:
1. Severe and acute onset of excruciating
retrosternal chest pain
2. Odynophagia
3. Positive Hamman sign, a crunching
heard upon palpation of the thorax due
to subcutaneous emphysema
4. Pain that can radiate to the left shoulder
4. ◾ Boerhaave syndrome
◾ is a full thickness tear secondary to extreme
retching and vomiting.
◾ It is most commonly tested in the setting of
an alcoholic.The most common location is at
the left posterolateral aspect of the distal
esophagus.
◾ Mallory-Weiss syndrome
◾ is a mucosal tear and is also due to
vomiting.
◾ It is not a perforation.The most common
location is at the gastroesophageal junction.
5. ◾ Surgical exploration with debridement of the
mediastinum and closure of the perforation is an
absolute emergency.
◾ Mediastinitis is a complication that carries a very
high mortality rate
6.
7.
8. Submucosal dissection of the esophagus
in patient with endoscopy for ERCP
and "difficulty passing scope."
Gastrografin swallow demonstrates
intramural dissection of the esophagus
from submucosal passage of endoscope
with appearance similar to aortic
dissection and "true and false lumen."
Arrows point to "false lumen" created
by passage of endoscope.
9. esophagram depict contrast extravasation from the
distal esophagus in a patient with spontaneous
perforation of the esophagus
10. Spontaneous, full-thickness rupture of the distal
thoracic esophagus
Associated with vomiting often following
consumption of large quantities of alcohol in
young people
Can occur during endoscopic examinations (75%
of adult cases)
Serious complication of bulimia
11. Symptoms
◾ sudden-onset, severe, retrosternal chest pain
◾ difficulty or painful swallowing
◾ hematemesis
though more common in Mallory-Weiss tears
Physical exam
◾ pleuritic chest pain
◾ hyperventilation
◾ tachycardia
12. ChestCT
◾ left-sided hydropneumothorax
◾ pneumomediastinum
◾ esophageal thickening
Contrast studies
◾ may show leakage from esophageal tear
use water-soluble contrast agent
(Gastrografin)
13. Medical management
conservative therapy
indicated in mild cases with stable patient and includes
intravenous resuscitation
nasogastric suction
NPO
prophylactic antibiotics- usually broad-coverage to
prevent mediastinal infection- imipenim or cilastin
Surgical intervention
surgical repair of perforation considered standard of
care
indicated depending on severity of tear and timing of
diagnosis
14.
15.
16.
17.
18. ◾ The most accurate test is an esophogram
(Gastrografin;); it will show leakage of contrast
outside of the esophagus.
◾ Barium cannot be used because it is caustic to
the tissues.
19. ◾ Mallory-Weiss tear presents with upper gastrointestinal
bleeding after prolonged or severe vomiting or retching.
◾ Repeated retching is followed by hematemesis of
bright red blood, or by black stool.
◾ MalloryWeiss does not present with dysphagia.There is
no specific therapy, and it will resolve spontaneously.
◾ Severe cases with persistent bleeding are managed
with an injection of epinephrine to stop bleeding or the
use of electrocautery.
Boerhaave syndrome is full penetration of the esophagus.
20. Strong, non-peristaltic contractions of the
esophageal body
Often precipitated by by ingestion of hot and
cold liquids
Patients have normal sphincter function
Associated withGERD
21.
22. • Symptoms
• symptoms may occur following ingestion of cold liquids
and include
• difficulty swallowing
• painful swallowing
• sudden onset chest pain not related to exertion
• spontaneous and radiated to back, ears, and neck
• Physical exam
• symptomatic relief with nitroglycerin
23. Evaluation
•UpperGI/esophageal contrast study
• shows "corkscrew esophagus"
•Manometry
• may show high-amplitude, simultaneous
contractions (non- peristaltic)
•Endoscopy - normal
•ECG - normal
•Stress test - normal
24. Medical management
symptomatic relief
antacids forGERD
nitrates for chest pain/spasms
calcium channel blockers
Surgical intervention
long esophagomyotomy
indicated for severe, incapacitating symptoms
25. ◾ Metaplasia of the squamous cell architecture of
the esophagus to glandular architecture
◾ A complication of chronicGERD
26. Biopsy
glandular metaplasia of distal esophagus
presence of stomach acid resutls in conversion of
normal squamous cells into columnar and goblet
cells (normally found in stomach and small
intestine)
27.
28. ◾ Ulceration leading to formation of stricture
◾ Increased risk of esophageal adenocarcinoma
29. ◾ Motor disorder of the distal esophagus caused by
degeneration ofAurbach's plexus
the most common motility disorder
◾ Pathophysiology
autoimmune process causes loss of NO-producing
neurons which normally relax the sphincter muscles
▪ association with HLA-DQw1
leads to failure of the LES to relax during swallowing
results in loss of peristalsis
ACHALASIA
30. Associated with
Chagas' disease
amastigotes destroy
ganglion cells
Scleroderma presents in
70% of these patients
◾ Epidemiology
more common in people under 50 years of age
ACHALASIA
32. ◾ Barium swallow may
show
narrowing of the
distal esophagus
loss of peristalsis in the
distal two thirds
dilated proximal esophagus
classic "bird's beak"
tapering at the esophageal
sphincter
33. most accurate test that may show
◾ increased LES pressure
◾ inability of LES to relax
◾ decreased peristalsis in the esophageal
body
◾ diffuse esophageal spasm
34.
35. ◾ useful in excluding secondary causes of
achalasia (i.e. malignancy)
◾ use to rule out malignancy
◾ shows normal mucosa
36. medications to reduce LES tone
1. nifedipine
2. nitrates
3. CCBs
4. botulinum toxin injections
▪ wears off in approximately 3-6 months
▪ requires reinjection
37. endoscopic balloon dilation of LES
▪ cures 80%
▪ leads to perforation in < 3% of patients
myotomy with fundoplication
▪ more effective and dangerous than
pneumatic dilation
38. ◾ Prognosis
medical and surgical outcomes are similar
often require multiple treatments
◾ Prevention
no preventive measures are available at this time
◾ Complications
esophageal malignancy secondary to Barrett's
esophagus secondary to chronicGERD
39. ◾ Pharyngeal pouch that develops in the proximal
esophageal wall
◾ Pulsion diverticula involving only the mucosa
located between thyropharyngeal and cricopharyngeus
muscle
◾ Etiology remains unknown, however, some have
suggested the causes to be related to structural or
physiological abnormalities of the cricopharyngeus
◾ Epidemiology
incidence unknown
most often occurs in age group (>70 years old)
40.
41. ◾ Symptoms
◾ dysphagia
◾ regurgitation
◾ choking
◾ chronic cough
◾ bad breath (halitosis)
◾ Physical exam
◾ palpable, fluctuant neck mass may be appreciable
42. Diagnosis is based highly on clinical
observations and patient history
Avoid upper endoscopy if known or
highly suspicious due to risk of rupture
Barium swallow
confirms diagnosis by visualizing pharyngeal
outpouch
43. myotomy of cricopharyngeus muscle
-with diverticula resection
- endoscopic has better success rates
compared to external approach
44. ◾ Complications surgery can lead to significant
complications including death given location of
lesion and age/health of average patient
population with this pathology
-may develop carcinoma within the pouch if not
resected
45. ◾ Small, thin web-like tissue growth partially
obstruct the upper esophagus
◾ Characterized by atrophic glossitis, esophageal
webs, and anemia
◾ Etiology unknown
◾ Epidemiology
most commonly observed in elderly woman
associated with chronic iron-deficiency anemia
◾ Patients at increased risk of developing
squamous cell carcinoma of the esophagus
47. Diagnosis can be aided by clinical observations,
including skin and nail changes
Upper endoscopy
may identify esophageal webs
CBC
may indicated chronic anemia
Fe studies
show Fe deficiency
48. ◾ Fe supplementation
indicated to treat chronic anemia state
◾ esophageal dilation
can be performed concurrently with upper
GI endoscopy or manometry
most commonly done with radial expansion
balloon method
49. ◾ Prognosis
most patients respond to treatment
◾ Prevention
Fe supplementation in patients with known anemia may
prevent web development
◾ Complications
bleeding may occur secondary to esophageal tear during
dilation
esophageal carcinoma
50. ◾Herniation of the stomach through the diaphragm into
the chest cavity
Type I
sliding hiatal hernia
◾ most common type (>95%)
◾ occurs at theGE junction
◾ stomach slides into the mediastinum
Type II
paraesophageal hiatal hernia (<5%)
◾ herniation of stomach fundus through diaphragm
◾ GE junction remains below diaphragm
◾ parallel to the esophagus
◾ Associated withGERD in 80% of sliding hiatal hernia
51.
52. ◾ Symptoms
may be asymptomatic, usually
identified incidentally on radiography
chest pain
heart burn
GERD
◾ Physical exam
◾ usually no significant findings
53. ◾ Barium swallow
- may observe stomach in chest cavity
◾ Usually an incidental finding
54.
55. Medical management
◾
◾ symptom management and lifestyle
modifications
indicated in type I (sliding hiatal hernias) to
relieveGERD symptoms
antacids
weight loss
dieting
Surgical intervention -surgical repair
indicated in type II (paraesophageal cases) due
to risk of strangulation
57. Schatzki ring
"Steakhouse syndrome" = dysphagia from solid
food associated with Schatzki ring
Schatzki ring is often from acid reflux and is
associated with hiatal hernia. This is a type of
scarring or tightening (also called peptic stricture)
of the distal esophagus.
Schatzki ring is associated with intermittent
dysphagia and is treated with pneumatic
dilation in an endoscopic procedure
58.
59. Corrosive Esophagitis
Caused by ingestion of strongly acidic or basic
chemical
◾ Lye, HCl
Results in
◾ esophageal perforation
◾ esophageal stricture formation Often
seen in suicide attempts or in the
pediatric population
60. Infectious Esophagitis
•Commonly seen inAIDS patients and
the Immunocompromised
•May be viral or fungal
• HSV (punched out lesions on EGD)
• CMV (large solitary ulcers or
erosions on EGD)
• Candida (white mucosal plaque-
like lesions on EGD)
•Odynophagia is main symptom
61. These pills cause esophagitis if in prolonged
contact:
• Doxycycline
• Alendronate
• KCI
Pills esophagitis
62. "What Is the Most Likely Diagnosis?"
Look for:
Age 50 or older
Dysphagia first for solids, followed later
(progressing) to dysphagia for liquids
Association with prolonged alcohol and
tobacco use
More than 5-10 years ofGERD symptoms
63.
64. 1.Endoscopy is indispensible, since only a biopsy can
diagnose cancer.
2.Barium might be the "best initial test," but no radiologic
test can diagnose cancer.
3.CT and MRI scans are not enough to diagnose esophageal
cancer; they are used to determine the extent of spread into
the surrounding tissues.
4.PET scan is used to determine the contents of anatomic
lesions if you are not certain whether they contain cancer.
PET scan is often used to determine whether a cancer is
resectable. Local disease is resectable, and widely
metastatic disease is not.
65. 1.No resection (removal) = no cure.Surgical
resection is always the thing to try.
2.Chemotherapy and radiation are used in
addition to surgical removal.
3.Stent placement is used for lesions that
cannot be resected surgically just to
keep the esophagus open for palliation and to
improve dysphagia
66. ◾ These patients present with symptoms of reflux
and have a clear history of scleroderma, or
progressive systemic sclerosis.
◾ Manometry shows decreased lower esophageal
sphincter pressure from an inability to close the
LES.
◾ The management is with PPis as it would be for
any person with reflux symptoms.
◾ The disorder is simply one of mechanical
immobility of the esophagus .
67. ◾ Esophageal smooth muscle atrophydecrease
LES pressure and dysmotilityacid reflux and
dysphagia stricture,Barrett esophagus, and
aspiration.
◾ Part ofCREST syndrome.
68. Manometry is the answer for:
1. Achalasia
2. Spasm
3. Scleroderma