Dysphagia Syndrome

2. dysphagia syndrome

3. Dysphagy
Dysphagia - a violation of the act of swallowing, w
hich is caused by organic or functional obstacle
to the promotion of food through the esophagus
.
The symptom is often defined as a feeling of bei
ng stuck in the throat. When dysphagia patient
can not swallow solid food at first, and then the l
iquid. Temporary dysphagia occurs in hysterical
neurosis.

5. Diseases of the esophagus accompanied b
y dysphagia:
• Esophageal dysmotility
• Esophageal diverticulum
• Congenital esophageal diaphragm membrane
• Benign tumors of the esophagus
• Esophageal cancer
• Post-burn esophageal stricture
• Foreign bodies of the esophagus
• Reflux esophagitis

6. Esophageal dysmotility
Achalasia - neuromuscular disease throughout t
he smooth muscle of the esophagus, esophage
al peristalsis manifested indiscriminate, mass vi
olation of the passage of food into the stomach,
persistent violation of the reflex opening of the l
ower esophageal sphincter during swallowing, d
ysphagia.
Clinical picture. For achalasia is characterized b
y a triad of symptoms: dysphagia, regurgitation,
pain.

7. Esophageal dysmotility
Achalasia
Diagnostics. Radiologically with achalasia termi
nal esophagus usually has a rounded shape, it
narrowed portion is often eccentric, characteristi
c symptom of overhanging wall of the esophagu
s above the narrowing.

10. Esophageal dysmotility
Achalasia
For the treatment of achalasia is used endoscopi
c balloon dilatation of the lower holes of the eso
phagus (gastric cardia).

12. Esophageal dysmotility
Cardiospasm
It is believed that when cardiospasm affected par
asympathetic system, mainly unit-intramural Au
erbach's plexus, and the fibers of the vagus ner
ve. As a result, damage to the nervous reflex ar
c reflex impaired opening of the cardia.
Often there is a history of an indication of the rel
ationship of symptoms with severe trauma or ex
periences. Typically, patients complain of dysph
agia is usually a long-term.

13. Esophageal dysmotility
Diagnostics. Typical radiological signs cardiosp
asm serve as an extension to a greater or lesse
r extent of the esophagus and the presence of "
narrow segment" in the field of physiological car
dia.

15. Esophageal dysmotility
Treatment. The main treatment is to expand car
diospasm physiological cardia cardio pneumatic
dilators.

17. Esophageal dysmotility
Esophageal spasm
Esophageal spasm - a disease of the esophagu
s caused by spastic contractions of its walls wit
h the normal function of the lower esophageal s
phincter.
A number of patients due to esophageal spasm
viscero-visceral reflexes, and combined with oth
er diseases.

18. Esophageal dysmotility
Esophageal spasm
Clinical picture. In the primary diffuse esophagospasm
permanent dysphagia, sometimes having a paradoxic
al character: hard and rough food passes smoothly, an
d the liquid and semi-liquid, on the contrary, it may be
delayed. Indirect signs include increased salivation, ra
pid reduction in body weight of the patient, increasing
weakness and anemia. Intermittent chest pain with no
specific relationship with food and disappearing for lon
g periods of remission to distinguish the clinical course
of the diffuse esophageal spasm and achalasia cardio
spasm.

19. Esophageal dysmotility
Esophageal spasm
Diagnostics. When X-ray the esophagus has a
deformation in the form of beads, pseudodiverti
culum, corkscrew; its diameter above and belo
w the constriction is not changed.

20. Esophageal spasm

21. Esophageal dysmotility
Esophageal spasm
Treatment. An effective method is the only complex of t
herapeutic measures, including:
- antispasmodic drugs - Halidorum of 0.05 g 3-4 times
a day, Nospanum - of 0.04 g 3-4 times a day - antipsy
chotics and tranquilizers - eglonil 100 mg intramuscula
rly 1 once a day for 7-10 days, - vitamins B6 (5% soluti
on to 1 ml of 1 per day intramuscularly) and B12 (0.01
% solution of 1 ml of 1 per day intramuscularly);
- The influence of acupuncture on points of general and l
ocal impact - 7-10 procedures course.

22. Esophageal diverticulum
The most common thoracic esophageal divertic
ula-bifurcation, slightly less - Zenker. Among pat
ients much dominated by men. In most cases, t
he pathology occurs in adulthood - from 40 to 6
0 years.

23. Esophageal diverticulum
Clinical picture. Diverticulum in the initial stage
can manifest only vague "discomfort" (some aw
kwardness when swallowing, periodically "scrap
e" in the throat). By increasing the size of the b
ag symptoms become richer. As a result of fallin
g food and compression of the esophagus diver
ticulum appears dysphagia, which is facilitated
after emptying diverticulum. After the meal, esp
ecially when lying down, there is a regurgitation
of undigested food mass from the diverticulum;
the patient has halitosis.

24. Esophageal diverticulum
Diagnostics. In recognition of diverticula radiolo
gical research plays a major role. Displaying a t
horough, multi-axis research in different positio
ns of the patient.

26. Esophageal diverticulum
• Treatment. Conservative treatment is indicate
d with small diverticula quickly defecate without
signs of diverticulitis, with scant clinical picture.
• Surgical treatment is indicated for complications
of esophageal diverticulum.

27. Congenital diaphragm membrane of the esop
hagus.
The diaphragm consists of connective tissue cove
red by keratinized epithelium. This diaphragm o
ften have holes through which can penetrate th
e food. Almost always localized in the upper par
t of the esophagus is much less - in the middle
section.

28. Congenital diaphragm membrane of the esop
hagus.
Clinical picture : The main clinical manifestation
is dysphagia, which occurs when introduced int
o the diet of the child solid food. When large hol
es in the membrane of food can fall into the sto
mach. These patients tend to chew everything t
horoughly than prevent food getting stuck in the
esophagus. The membrane under the influence
of food debris often inflamed

29. Diagnosis: Clinical manifestations
The contrast study of the esophagus

30. Congenital diaphragm membrane of the esop
hagus.
Treatment: The gradual expansion of the es
ophagus probes of different diameters. W
hen the diaphragm completely covers the
clearance necessary to remove it under e
ndoscopic control.

31. Benign tumors of the esophagus.
Tumors with respect to the wall of the esophagus
may be intraluminal (polypoid), and the intramur
al.

32. Benign tumors of the esophagus.
Clinical picture. The most common symptom is a slowl
y increasing over the years, dysphagia. When intramur
al tumors, circularly covering the esophagus, dysphagi
a may be permanent, sometimes patients report pain,
feeling of pressure in the chest or overflow. Bleeding a
nd anemia due to traumatization polyps due to their ex
cessive mobility at the intramural tumors - the extende
d damage and anemic esophageal mucosa over the tu
mor. Symptoms characteristic of mediastinal tumors, a
re due to compression of mediastinal organs (dyspnea
, cough, palpitation, cyanosis, arrhythmias, and others.
).

33. Benign tumors of the esophagus.
Diagnostics. The main method of diagnosis of b
enign tumors of the esophagus is an X-ray exa
mination. Characterized by the following radiolo
gical signs: clearly defined oval filling defect on
one of the walls of the esophagus, stored relief
of the mucosa and the elasticity of the walls of t
he esophagus in the area of defects detected in
an oblique position clear angle between the wall
and the edge of esophageal cancer (a symptom
of "hood").

35. Benign tumors of the esophagus.
Treatment. The diagnosis of esophageal polyp is
an indication for surgery to remove it because o
f the risk of complications such as bleeding and
malignancy. Malignancy of polyps (even small s
ize) is often observed.

36. Cancer of the esophagus.
Esophageal cancer is one of the most common c
ancer sites. With age, the incidence of esophag
eal cancer is increasing; most often they becom
e ill people over 60 years. In men, cancer of the
esophagus is observed 2-3 times more often th
an women.

37. Cancer of the esophagus.
There are three major forms of esophageal canc
er: Ulcerative (saucer), nodular (mushroom, war
ty - papillomatouz) and infiltrative cancer.

38. Cancer of the esophagus.
Clinical picture. The clinical picture of esophageal can
cer can be divided into two groups of symptoms - local
, depending on the destruction of the walls of the esop
hagus and surrounding organs, and general. In most c
ases, the first symptom of cancer is esophageal dysph
agia. For cancer of the esophagus is characterized by
a progressive increase in obstruction of the esophagu
s, which in some patients develop quickly, while others
- slowly. Initially stuck rough, poorly chewed food. In th
e future, no longer held even well-chewed food, and p
atients have to take a semi-liquid and liquid food. Som
etimes observed periods to improve patency of food af
ter a period of persistent dysphagia commonly associa
ted with the collapse of the tumor.

39. Cancer of the esophagus.
Diagnostics. The main role in the diagnosis of e
sophageal cancer belongs to the X-ray methods
. Esophagoscopy is shown in all cases of suspe
cted cancer of the esophagus. The objective of
the study is not only to visually confirm the diag
nosis of esophageal cancer, but also to obtain h
istological confirmation of the diagnosis.

41. Cancer of the esophagus.
Treatment of esophageal cancer is currently radi
cal surgery is usually preceded by preoperative
radiotherapy.

42. Post-burn, scar stricture of the esophag
us.
Chemical burn esophagus is most often the result
of accidental or, rarely, suicidal for admission ac
ids (usually vinegar essence) or alkalis (usually
caustic soda).

43. Post-burn, scar stricture of the esophag
us.
The clinical picture of burns esophagus varies accordi
ngly the development of pathological changes in its wa
ll and can be divided into four periods: 1) acute, which
lasts up to two weeks and is characterized by necrosis
mortem in the wall of the esophagus; 2) the period of t
he alleged welfare 2-3 weeks, when there is a rejectio
n of necrotic tissue; 3) during the formation of scar con
traction (from 3-4 weeks), during which there is a deve
lopment of granulation, the process of epithelialization
and the formation of strictures; 4) the period of formed
scar stricture (2 to 6 months).

44. Post-burn, scar stricture of the esophag
us.
Diagnostics. Usually the diagnosis is already se
t on the basis of clinical history. X-ray examinati
on and endoscopy allow to specify the extent, lo
cation and extent of the restriction.

46. Post-burn, scar stricture of the esophag
us.
Treatment. The main task - to start therapeutic
measures as soon as possible. At present, it pr
oved the feasibility of early boogieing (ranging fr
om 8-10 days after the burn), which should be c
arried out for 1-1,5 months. At the same time ap
point lidasa injections for 12 days.

47. Foreign bodies of the esophagus.
The clinical picture. Symptoms depend on the
nature of the foreign body, the level of its delays
in the esophagus, the degree of damage to the
wall of the esophagus. Common symptoms are
dysphagia, which is caused by a foreign body, t
he development of esophageal spasm of muscl
es and inflammatory reaction of the mucous me
mbrane of the esophagus. The result is a compl
ete obstruction of the esophagus and regurgitati
on when receiving liquid or food.

48. Foreign bodies of the esophagus.
Diagnostics. Emergency X-ray detect metallic for
eign bodies, low contrast detect foreign bodies i
n the study of the esophagus with a water-solub
le contrast agent.

50. Foreign bodies of the esophagus.
Treatment. If you suspect a foreign body of the e
sophagus of the patient is necessary at any tim
e to send a surgical hospital. Removal of foreig
n body is carried out with the help of hard Esop
hagoscopy and a set of special tools. If unable t
o retrieve a foreign body through esophagoscop
e shows the operation - a dissection of the esop
hagus, foreign body removal and closure of the
esophageal wall.

51. Reflux esophagitis.
The disease is caused by repeated prolonged ex
posure to the mucosa of the esophagus of gastr
ic juice, bile, pancreatic juice. The disease suba
cute or chronic. The cause of reflux esophagitis
is gastroesophageal reflux, which is associated
with the violation of closing function of the lower
esophageal sphincter.

52. Reflux esophagitis.
The clinical picture. Patients worried about hear
tburn, a burning sensation behind the breastbon
e or in the course of the esophagus that occur o
r are aggravated by tilting the torso forward (goi
ng abandonment of gastric juice in the mouth),
due to the impact of pain on the inflamed muco
sa of the esophagus gastric juice and bile, belc
hing. Pain may be associated with severe spast
ic contractions of the esophagus.

54. Reflux esophagitis.
Diagnostics. Diagnosis of reflux oesophagitis es
tablish the presence of the characteristic sympt
oms of patients with the disease. X-rays (especi
ally in the supine position) can detect gastroeso
phageal reflux symptoms of esophagitis.

56. Reflux esophagitis.
Treatment. The primary activity is to treat the un
derlying disease, the conditions for gastroesoph
ageal reflux (hiatal hernia, pyloroduodenal sten
osis, pilorospazm). Depending on the stage of e
sophagitis appoint a mechanically and chemical
ly sparing diet, food fractions (4-6 times a day),
the last meal - for 3-4 hours before bedtime. As
sign Blockers H2-receptor, alkalizing, envelopin
g, astringents, antispasmodics; metoclopramide
(Reglan), local anesthetics, sedatives, antihista
mines, vitamins; not recommended the use of al
cohol and smoking.

59. Esophagus bleedi
ng syndrome

60. Common Causes of Esophagus Blee
ding
• Esophageal varices
• Mallory-Weiss tear
• Erosive esophagitis
• Barrett's esophagus

61. Mallory-Weiss Tear
(MWT )
Synonyms, gastroesophageal tears,
Mallory-Weiss syndrome, Mallory-Wei
ss lesion

62. Mallory-Weiss syndrome - is a lon
gitudinal gap of the mucous memb
rane of the gastrointestinal tract in
the esophagogastric junction that
occurs when a strong urge to vomi
t or vomiting during the most.
A Mallory-Weiss tear occurs in th
e mucous membrane where the
esophagus connects to the sto
mach. The tear causes bleedin
g.

64. Frequency:
• MWTs account for 1-15% of cases of
upper gastrointestinal bleeding.

65. Mortality/Morbidity:
• Bleeding from MWTs stops spontaneously in 80-90%
of patients. With conservative therapy, most tears heal
uneventfully within 48 hours. Thus, a MWT can easily
be missed if endoscopy is delayed.
• The degree of blood loss varies. Earlier studies report
ed that the proportion of patients requiring blood transf
usions was 40-70%. These figures do not seem to be t
he trend today and are probably significantly lower.
• Hemodynamic instability and shock may occur in up to
10% of patients. In one series, mortality as high as 8.6
% was attributed to MWTs. Current clinical experience
suggests a significantly lower mortality rate from MWT
s.

66. Causes
• retching and vomiting itself.
• hiccough
• cough
• blunt abdominal trauma.
• alcoholism
• pregnancy
• diaphragmatic hernia

67. Symptoms
• MWTs do not elicit specific physical signs.
• Classically, the disease manifested blood in vo
mit (hematemesis) that appear after repeated b
outs of vomiting or retching. However, the typic
al pattern observed in only 30-50% of patients.
• Less common symptoms include melena, unch
anged presence of blood in the stool, syncope,
and abdominal pain.

68. Exams and Tests
• EGD (esophagogastroduodenoscopy) showing a tear
with bleeding
• Hemoglobin and hematocrit studies are performed to a
ssess the severity of the initial bleeding episode and to
monitor patients.
• Platelet count, prothrombin time, and activated partial t
hromboplastin time are performed to assess for sever
e thrombocytopenia and coagulopathy as complicating
issues. Coagulation studies are needed in patients on
anticoagulants or with minimal or no oral intake while
on antibiotics. Platelet count may be low because of al
cohol use.
• Creatinine and electrolyte levels are measured to guid
e intravenous fluid therapy.
• Blood type and antibody screen are obtained for poten
tial blood transfusions.

69. Mallory-Weiss tear. Typical longitudinal mucosal tear wit
h overlying fibrinous exudate extending from the distal e
sophagus to the gastric cardia.

70. Mallory-Weiss tear. Retroflexed view of the cardia
showing the typical location of the tear with a clea
n base.

71. Other Tests:
• Electrocardiogram and cardiac enzymes (if indi
cated) - To assess for myocardial ischemia relat
ed to acute gastrointestinal blood loss, especiall
y in patients with significant anemia, hemodyna
mic instability, cardiovascular disease, coexistin
g chest pain, and/or advanced age.

72. treatment
- Conservative treatment consists in carrying out
intravenous fluid therapy to replenish the intrav
ascular volume. When severe blood loss may r
equire a transfusion of blood products.
- In order to reduce emesis administered antiem
etics (e.g. prochlorperazine 5-10 mg orally or i /
m 4 times per day (up to 40 mg / day)).
- Also prescribe drugs reduce gastric acidity (eg,
proton pump inhibitors - omeprazole (ITA Losek
, Ultop, Omez) 20 mg orally or esomeprazole (N
exium) at a dose of 20-40 mg orally for 2 weeks
.

73. treatment
- Antacids and enveloping means: sucralfate (V
enter) at a dose of 1 g orally four times a day fo
r 2 weeks).
- Since the purpose for bleeding a haemostatic p
robe set Sengstakena-Blackmoore, wherein the
solution is administered into the stomach the ad
renaline (epinephrine hydrochloride) or norepin
ephrine (0.1% solution 4 ml) together with 100-
150 ml of 5% solution aminocaproic acid (amino
hexanoic acid p-p 5%), or give the drink 1 tbsp t
he mixture every 15 minutes.

74. Esophageal varices

75. • Bleeding esophageal varices result from di
lated (wider than normal) veins in the walls of th
e lower part of the esophagus and sometimes t
he upper part of the stomach.
• They are most often a consequence of portal hy
pertension, such as may be seen with cirrhosis;
patients with esophageal varices have a strong
tendency to develop bleeding.

76. Esophageal varices are diagnosed with
endoscopy

77. Causes
The reasons for the vast majority of cases, varico
se veins of the esophagus are the state, accom
panied by the phenomenon of increasing the pr
essure in the vena cava - portal hypertension:
- diseases affecting the liver parenchyma (tumor
, cirrhosis, hydatid disease, amyloidosis) - ar
e more common in middle age;
- narrowing of the portal vein (due to multiple scl
erosis, thrombosis, compression of the outside)
- mostly diagnosed in young people;
-Chiari disease.

78. Symptoms
• Vomiting
• Vomiting blood
• Black, tarry stools
• Bloody stools
• Decreased urine output
• Symptoms of chronic liver disease (su
ch as cirrhosis)
• Excessive thirst
• Paleness
• Light-headedness

79. • Patients typically present with sudden, pai
nless, upper GI bleeding, often massive. S
igns of shock may be present. Bleeding is
usually from the distal esophagus, less oft
en from the gastric fundus. Bleeding from
gastric varices also may be acute but is m
ore often subacute or chronic.
• Bleeding into the GI tract may precipitate
hepatic encephalopathy in patients with im
paired hepatic function.

80. Exams and Tests
• Physical examination:
• Signs of chronic liver disease or ci
rrhosis
• Low blood pressure
• Rapid heart rate
• Bloody or black stool on rectal exa
m
• Endoscopy
• Evaluation for coagulopathy

81. Both esophageal and gastric varices are best di
agnosed by endoscopy, which may also identify
varices at high risk of bleeding (eg, those with r
ed markings).
Because varices are typically associated with si
gnificant hepatic disease, evaluation for possibl
e coagulopathy is important.
Laboratory tests include CBC with platelets, PT,
PTT, and liver function tests. Bleeding patients
should have type and crossmatch for 6 units of
packed RBCs.

82. Esophageal varices

83. Bleeding Esophageal Varix

84. Esophageal Varices

85. Esophageal varices seven days post ba
nding, showing ulceration at the site of
banding.

86. Treatment
• Treatment of the disease against which develop
ed varices (hepatitis, cirrhosis, strokes and so o
n.).
• Lifestyle (exercise should be excluded, not over
work, personal hygiene).
• Diet (strict diet recommended in the patient's un
derlying disease).
• Medication:

87. Treatment
• Medication:
1. agents that reduce the acidity in the stomach
- antacids;
2. binding agents;
3. vitamins.
• In the case of bleeding - blood transfusions, pla
sma, packed red blood cells, crystalloid and coll
oid solutions, vasoconstrictors, hemostatics me
dications.
• Surgical treatment in case of bleeding esophag
eal varices stitching, removing the vessels.

88. Barrett's esophagus (sometimes
called Barrett's syndrome, CELL
O, columnar epithelium lined lower
esophagus or colloquially as Barr
ett's) refers to an abnormal chang
e (metaplasia) in the cells of the lo
wer end of the esophagus thought
to be caused by damage from chr
onic acid exposure, or reflux esop
hagitis.

89. Barrett's esophagus is found in ab
out 10% of patients who seek med
ical care for heartburn (gastroesop
hageal reflux). It is considered to b
e a premalignant condition and is
associated with an increased risk
of esophageal cancer.

91. Barrett's esophagus is caused by
gastroesophageal reflux disease,
which allows the stomach's conten
ts to damage the cells lining the lo
wer esophagus. However, not ever
y person who has GERD will devel
op Barrett's esophagus.

92. Examiners are unable to predict w
hich heartburn sufferers will devel
op Barrett's esophagus. While ther
e is no relationship between the se
verity of heartburn and the develo
pment of Barrett's esophagus, ther
e is a relationship between chronic
heartburn and the development of
Barrett's esophagus.

93. Sometimes people with Barrett's esop
hagus will have no heartburn sympto
ms at all. In rare cases, damage to th
e esophagus may be caused by swall
owing a corrosive substance such as l
ye.
The change from normal to premalign
ant cells that indicates Barrett's esoph
agus does not cause any particular sy
mptoms. However, warning signs that
should not be ignored include:

94. Causes and Symptoms
• frequent and longstanding heartburn
• trouble swallowing (dysphagia)
• vomiting blood
• pain under the breastbone where the
esophagus meets the stomach
• unintentional weight loss because eati
ng is painful

95. • The metaplasia of
Barrett's esophag
us is visible grossl
y through a gastr
oscope.

96. Diagnosis
• By biopsy specimens must be confirm
ed by at least two for the true diagno
sis of Barrett's.

97. Treatment
• First of all, you need to give up eating, snacking
at night, after a meal in any case can not lie. In
hyperalimentation an increase in the volume of t
he stomach, which leads to relaxation of the es
ophageal sphincter and gastroesophageal reflu
x.
• Fully refuse to carbonated beverages, including
Coca - Cola, as well as alcoholic beverages; of
butter, margarine, spread. The food must be tak
en in small portions, 4 times a day, 30 minutes
after a meal needed a walk in the fresh air. Foo
d should be rich in protein.

98. Treatment
• The main methods of treatment include the use
of proton pump inhibitors Omeprazole 40 mg 1 t
ime a day, rabeprazole 40 mg 1 time a day, lans
oprazole 60 mg 1 time a day.
• vitamins E, C, coenzyme Q10.
• endoscopic techniques,
• surgical interventions.