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ESOPHAGEAL
DISORDER
DR JABBAR JASIM
2023
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
 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
◾ 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.
◾ 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
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.
esophagram depict contrast extravasation from the
distal esophagus in a patient with spontaneous
perforation of the esophagus
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
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
ChestCT
◾ left-sided hydropneumothorax
◾ pneumomediastinum
◾ esophageal thickening
Contrast studies
◾ may show leakage from esophageal tear
use water-soluble contrast agent
(Gastrografin)
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
◾ 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.
◾ 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.
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
• 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
Evaluation
•UpperGI/esophageal contrast study
• shows "corkscrew esophagus"
•Manometry
• may show high-amplitude, simultaneous
contractions (non- peristaltic)
•Endoscopy - normal
•ECG - normal
•Stress test - normal
Medical management
 symptomatic relief
 antacids forGERD
 nitrates for chest pain/spasms
 calcium channel blockers
Surgical intervention
 long esophagomyotomy
 indicated for severe, incapacitating symptoms
◾ Metaplasia of the squamous cell architecture of
the esophagus to glandular architecture
◾ A complication of chronicGERD
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)
◾ Ulceration leading to formation of stricture
◾ Increased risk of esophageal adenocarcinoma
◾ 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
 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
◾ Symptoms
 dysphagia for solids and liquids
▪ usually worse for liquids
 weight loss
◾ 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
most accurate test that may show
◾ increased LES pressure
◾ inability of LES to relax
◾ decreased peristalsis in the esophageal
body
◾ diffuse esophageal spasm
◾ useful in excluding secondary causes of
achalasia (i.e. malignancy)
◾ use to rule out malignancy
◾ shows normal mucosa
 medications to reduce LES tone
1. nifedipine
2. nitrates
3. CCBs
4. botulinum toxin injections
▪ wears off in approximately 3-6 months
▪ requires reinjection
 endoscopic balloon dilation of LES
▪ cures 80%
▪ leads to perforation in < 3% of patients
 myotomy with fundoplication
▪ more effective and dangerous than
pneumatic dilation
◾ 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
◾ 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)
◾ Symptoms
◾ dysphagia
◾ regurgitation
◾ choking
◾ chronic cough
◾ bad breath (halitosis)
◾ Physical exam
◾ palpable, fluctuant neck mass may be appreciable
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
 myotomy of cricopharyngeus muscle
 -with diverticula resection
 - endoscopic has better success rates
compared to external approach
◾ 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
◾ 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
Symptoms
◾ difficulty swallowing
◾ chronic cough
◾ weakness/malaise
◾ nail changes
Physical exam
◾ atrophic glossitis
◾ esophageal webs
◾ anemia
◾ spoon nail deformitie
 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
◾ 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
◾ 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
◾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
◾ Symptoms
 may be asymptomatic, usually
identified incidentally on radiography
 chest pain
 heart burn
 GERD
◾ Physical exam
◾ usually no significant findings
◾ Barium swallow
- may observe stomach in chest cavity
◾ Usually an incidental finding
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
Prognosis
◾ treatment relieves most symptoms
Prevention
◾ lifestyle modifications can prevent symptoms
Complications
◾ aspirate pneumonia
◾ gastric strangulation
◾ iron-deficiency/malnutrition
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
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
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
These pills cause esophagitis if in prolonged
contact:
• Doxycycline
• Alendronate
• KCI
Pills esophagitis
"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
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.
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
◾ 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 .
◾ Esophageal smooth muscle atrophydecrease
LES pressure and dysmotilityacid reflux and
dysphagia stricture,Barrett esophagus, and
aspiration.
◾ Part ofCREST syndrome.
Manometry is the answer for:
1. Achalasia
2. Spasm
3. Scleroderma
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4-esophageal disease.pptx

  • 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
  • 31. ◾ Symptoms  dysphagia for solids and liquids ▪ usually worse for liquids  weight loss
  • 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
  • 46. Symptoms ◾ difficulty swallowing ◾ chronic cough ◾ weakness/malaise ◾ nail changes Physical exam ◾ atrophic glossitis ◾ esophageal webs ◾ anemia ◾ spoon nail deformitie
  • 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
  • 56. Prognosis ◾ treatment relieves most symptoms Prevention ◾ lifestyle modifications can prevent symptoms Complications ◾ aspirate pneumonia ◾ gastric strangulation ◾ iron-deficiency/malnutrition
  • 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 atrophydecrease LES pressure and dysmotilityacid reflux and dysphagia stricture,Barrett esophagus, and aspiration. ◾ Part ofCREST syndrome.
  • 68. Manometry is the answer for: 1. Achalasia 2. Spasm 3. Scleroderma