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8/9/2019 TBL 3 - Dysphagia
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TBL 3: DYSPHAGIA
By: Anis, Aishah, Nubla, Hanafi, Hidayah
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Dysphagia: is a difficulty in swallowing and always
need investigation to exclude malignancy.
Odynophagia: is painfull while swallowing in themouth or oesophagus
Globus hystericus :The sensation of having a lump in
the throat when there is nothing there
If symptoms are progressive or prolonged thenurgent investigation is required.
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HOW TO TAKE HISTORY?
Dysphagia
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History
Duration
Progression
Aggravating factorRelieving factor
Level
Vomiting history
Saliva accumulation
Heartburn
Belching
LOWLOA
SOB
Cough
hemoptysis
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Physical Examination
Inspection
Mouth
Ulcer Swelling -tonsil
Hydration status
Neck
Swelling or mass
Lymph node
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Abdominal examination
Respiratory examination
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Causes of Dysphagia - Mural
Ca esophagus Progressive cause, LOW, anorexia, low-
grade anemia, small hematemesis
Reflux esophagitis
& stricture
Preceded by heartburn, progressive course,
nocturnal regurgitationAchalasia Frequent regurgitation, recurrent chest
infection
Tracheo-esophageal
fistula
Recurrent chest infection, coughing after
drinkingCaustic stricture Examination shows corrosive ingestion,
chronic dysphagia
Scleroderma Slow onset, a/w skin and hair changes
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Causes of Dysphagia - Intraluminal
Foreign body Acute onset, marked retrosternal dicomfort,
dysphagia even to saliva
Causes of Dysphagia - Extramural
Pulsion
diverticulum
Intermittent symptoms, unexpected regurgitation
External
compression
Mediastinal lymph nodes, left arterial
hyperthrophy, bronchial malignancy
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Risk Factors for Oesophageal Ca
Squamous cell carcinoma Adenocarcinoma
1. Heavy alcohol intake
2. Smoker
3. Poor diet- low intake offruit and vegetables
1. Poor diet- low intake of
fruit and vegetables
2. Acid suppressingmedications
3. Peptic oesophagitis and
stricture
4. Achalasia
5. Oesophageal web/
pharyngeal pouch
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INVESTIGATIONS
By: Aishah Azman
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Investigations
Full blood count (FBC)
Liver function test (LFT)
Renal profile Chest Xray& CT scan
Oesophageal-gastric-duodenal scopy (OGDS)
Barium swallow
Esophageal monometry
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Full Blood Count
Anaemia Tumours much more commonly cause this
rather than reflux
Test Result interpretation
Hemoglobin 10.4 Low
Hematocrit 31.1 Low
Mean Corpuscular
Hemoglobin (MC
H)
26. 2 Low
Platelets 595 High
RBC Dist Width 15.2 High
Total RBC 3.95 Low
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Liver Function Test
Looking out for any hepatic disease or involvement
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Renal profile
To look for signs of dehydration
BUN 4.3 mmol/L N
Sodium 135.2 mmol/L N
Potassium 4.83 mmol/L NCreatinine 89 Umol/L N
Chloride 103.7 mmol/L N
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Chest X-ray and CT scan
To rule out external compression
Allow tumour staging
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OGDS
The study of choice for evaluating persistent
heartburn, dysphagia, odynophagia, and structural
abnormalities detected on barium esophagography.
In addition to direct visualization, it allows biopsy of
mucosal abnormalities and of normal mucosa (to
evaluate for eosinophilic esophagitis) as well as
dilation of strictures.
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Barium Swallow
Patients with esophageal dysphagia often are evaluated first with aradiographic barium study to differentiate between mechanicallesions and motility disorders, providing important information aboutthe latter in particular.
In patients with esophageal dysphagia and a suspected motilitydisorder, barium esophagoscopy should be obtained first.
In patients whom there is a high suspicion of a mechanical lesion,many clinicians will proceed first to endoscopic evaluation because itbetter identifies mucosa lesions and permits mucosal biopsy anddilation.
However, barium study is more sensitive for detecting subtleesophageal narrowing due to rings, achalasia, and proximalesophageal lesions.
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Esophageal Monometry
Used to assess oesophageal motility
Indication:
determining LES location to allow precise placement of
conventional electrode pH probe establishing the aetiology of dysphagia in patients in whom
a mechanical obstruction cannot be found, especially if adiagnosis of achalasia is suspected by endoscopy or bariumstudy
for the preoperative assessment of patients beingconsidered for antireflux surgery to exclude an alternativediagnosis (eg, achalasia) or possibly to assess peristalticfunction in the esophageal body.
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Investigations Gastro-esophageal
reflux disease (GERD)
Oesophagus ca Achalasia
Barium swallow reverse flow of bariuminto the lower end of
oesophagus (from the
stomach)
irregular, persistent,intrinsic feeling defect
-uniformly dilatedoesophagus above,
with a smooth tapering
segment below-
cucumber oesophagus
-chronic case, may be
sigmoid shape
Endoscopy red, angry looking
mucosa in the lower
end of the oesophagus
-Early stage: superficial
plaque or ulceration
-Advance: ulcerated
mass with stricture or
circumferential mass
or a large ulceration
dilated sac containing
stagnant food & fluid
due to stasis which
splashes out with each
heart beat & with each
respiratory movement
Oesophageal
manometry
- - -Hypertensive lower
oesophageal sphincter
(LOS)
-increase resting
pressure in oesophagus
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ACHALASIA
By: Aishah Azman
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Achalasia
The rhythmic contractions of the esophagusare greatly decreased, LES does not relaxnormally, and the resting pressure of the
lower esophageal sphincter is increased. Persons with achalasia lack non-adrenergic,
non-cholinergic, inhibitory ganglion cells,causing an imbalance in excitatory and
inhibitory neurotransmission. The result is ahypertensive non-relaxed esophagealsphincter.
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Etiology/Pathophysiology
Most common 1 esophageal motility disorder
Due to
absence of esophageal smooth muscle peristalsis
Increased lower esophageal sphincter (LES) restingpressure
Failure of LES to relax in response to a bolus of food.
Results in functional obstruction with esophageal
dilatation (Esophagus: widened, lengthened) Manifestation: 20-40 year old (May be seen in
infancy and early childhood)
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Achalasia vs other esophageal motility
disorders
Diffuse esophageal spasm: uncoordinated, high
amplitude esophageal contractions
Nutcracker esophageal: exceedingly high amplitude
esophageal contractions
Strictures: secondary to ingestion of caustic agents
or longstanding gastroesophageal reflux or
esophagitis
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Signs and symptoms
Progressive dysphagia (Solids and liquids)
Substernal chest pain
Regurgitation of undigested food
Weight loss Aspiration and respiratory symptoms secondary to
esophageal retention, regurgitation, and overflow intotrachea
Recurrent aspiration pneumonia Bloating
Inability to burp
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Diagnostic evaluation
CXR Mediastinal widening with possible air-fluid level
Barium esophagram Marked dilatation of esophagus
Narrowed, tapered bird beak distal esophagus
Longstanding: lengthened, tortuous esophagus (sigmoid esophagus)
Manometry (Gold standard) High LES resting pressure
Incomplete relaxation upon swallowing
Failure of peristalsis
*elevated resting pressure in the body of the esophagus may also be present Upper GI endoscopy with biopsy to rule out esophageal cancer,
esophagitis and strictures
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Treatment and Management
Medical therapy Eg. Ca channel blocker, nitrates, sildenafil
Short term improvement
Pneumatic dilatation of LES
>60% effective Botulinum toxin injections
Efficacy questionable
Must repeat every few months
Surgical treatment Esophagomyotomy (Heller myotomy) with
sectioning of the LES Prefer laparoscopy than open thoracotomy or laparotomy
Include anti-reflux procedure
Best: abdominal laparoscopic myotomy with an anti-reflux procedure
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Prognosis and Complication
Prognosis increased risk of esophageal ca
Pneumatic dilatation One: 60% effective
Two: 80% effective
Perforation: 2-15% (*increased with repeated dilatations andprior botox)
Botulinum injection 40% : not effective
Multiple injections
Scar: increase risk of complication following pneumatid dilatationor surgery
Surgery 3-4% : pneumothorax and esophageal mucosalperforation
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2. GORD
Gastro-oesophageal reflux is a condition caused by
the retrograde passage of gastric contents into the
oesophagus resulting in inflammation (oesophagitis),which manifests as dyspepsia. It manifests from the
lower pressure of the LOS.
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Causes of GORD
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Reflux OesophagitisSymptomatic esophagitis occur with:
Prolonged exposure of mucosa to excessive reflux,
both in number of episodes & volume.
Impaired normal mechanisms from clearing the loweresophagus.
High levels of acid & pepsin.
Presence of bile & pancreatic enzymes (alkalinereflux).
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Clinical Features
Retrosternal burning pain, radiating to epigastrium,jaw and arms. (Oesophageal pain is often confused
with cardiac pain.)
Triad (Heartburn, epigastric pain, regurgitation)
Regurgitation of acid contents into the mouth &execessive salive proir to reflux(waterbrash).
Back pain (a penetrating ulcer in Barretts
oesophagus). Dysphagia from a benign stricture.
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Pathophysiology
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The action of the lower esophageal sphincter (LES) isperhaps the most important factor (mechanism) forpreventing reflux.
The esophagus is a muscular tube that extends from thelower throat to the stomach. The LES is a specialized ringof muscle that surrounds the lower-most end of theesophagus where it joins the stomach. The muscle thatmakes up the LES is active most of the time.
This means that it is contracting and closing off thepassage from the esophagus into the stomach. This closingof the passage prevents reflux. When food or saliva isswallowed, the LES relaxes for a few seconds to allowthe food or saliva to pass from the esophagus into thestomach, and then it closes again.
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Several different abnormalities of the LES have been found inpatients with GERD. Two of them involve the function of theLES.
The first is abnormally weak contraction of the LES, which
reduces its ability to prevent reflux. The second is abnormal relaxations of the LES, called
transient LES relaxations.
They are abnormal in that they do not accompany swallowsand they last for a long time, up to several minutes. Theseprolonged relaxations allow reflux to occur more easily.
The transient LES relaxations occur in patients with GERD mostcommonly after meals when the stomach is distended withfood. Transient LES relaxations also occur in individuals withoutGERD, but they are infrequent.
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1. Metaplasia of distal esophagus to columnar
epithelium in persistent gastroesophageal reflux(mixture of gastric & intestinal type)
BARRETS ESOPHAGUS is defined as the presence of
glandular mucosa showing intestinal metaplasia.
Risk of adenocarcinoma (30 x)2. Peptic ulceration & fibrous stricture
3. Motility abnormality (abnormal peristalsis in loweresophagus decrease clearing & aggravate reflux
disease4. Oesophageal shortening
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Diagnostics measurement
24-hour pH recording is the gold standard
TLOSRs are the most important manometric findings
in GORD The length and pressure of the LOS are also
important
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3. Barret Oesophagitis
Metaplastic change in the lining mucosa of theoesophagus in response to chronic GORD
Junction between squamousoesophageal mucosa and
gastric mucosa moves proximally
Risk of adenocarcinoma (30 x)
Divided into:
Classic Barretts (3cm or more columnar epithelium)
Short-segment Barrets (less than 3cm) Cardiametaplasia (intestinal metaplasia at the
oesophagogastric junction without any macroscopic change at
endoscopy)41
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Causes & symptoms
Barrett's esophagus is caused by GERD whichallows the stomach's contents to damage the cellslining the lower esophagus
Warning signs Frequent and longstanding heartburn, dysphagia,
vomitting blood
Change of voices (laryngitis)
**it is a grade 4 esophagitis + displastic change
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The squamocolumnar junction, where the Barrett's
esophagus joins the normal squamous esophagus, is a
great distance from the bottom of the esophagus due
to the long segment of Barrett's esophagus
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The short segment of Barrett's esophagus is seen here as a strip or
"tongue" of red lining surrounded by normal pinkish-white squamous
lining. There is a small island of Barrett's esophagus, surrounded by
normal squamous lining, next to the tongue of Barrett's esophagus.
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Figure 17-6 Barrett esophagus.A, B, Gross view of distal esophagus (top) and proximastomach (bottom), showingA, the normal gastroesophageal junction (arrow) and C,Endoscopic view of Barrett esophagus showing red velvety gastrointestinal mucosaextending from the gastroesophageal orifice. Note the paler squamous esophageal mu
B, the granular zone of
Barrett esophagus
(arrow).
C, Endoscopic view
showing red velvety
gastrointestinal mucosa
extending from the
gastroesophageal orifice.
Barrett esophagus.
A, the normal gastro-
esophageal
junction (arrow)
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HIATUS HERNIA
By: Hidayah
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Hiatal Hernia48
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Hiatus Hernia
A protrusion of a portion of the stomach across the
opening in the diaphragm that the esophagus
normally passes through.
HH is common especially in women and with
advancing years
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Sliding HH PEH
(90% of cases): upwardmigration of the GEJ
through the esophageal
hiatus and into the thorax
Most often caused by
strecthing the esophageal
hiatus
is a rolling of the gastricfundus upward through the
esophageal hiatus into the
esophageal hiatus and ino
the thorax, with normalposition of the GEJ
It have a significantly
increased risk ofVOLVULUS &
STRANGULATION
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Classification
Type Hiatal Hernia
I Sliding H
II PEH
III I + II
IV Herniation of stomach &
additional intra-abdominalorgan: colon, spleen @ omentum
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Clinical features
Sliding HH Paraesophageal HH
1) Often asymptomatic
2) Incompetence of the
GEJ may result: REFLUX
causing symptoms of
GERD (e.g., heartburn,cough, regurgitation,
dysphagia)
1) Often asymtomatic
2) But may present with severe
ischemic symptoms if volvulus @
incarceration of the stomach occurs
3) Since the GEJ is intact, REFLUXRARELY occurs
4) OBSTRUCTIVE symptoms (e.g.,
dysphagia, postprandial fullness,
heartburn, dyspnea) may signalimpending volvulus
5) HEMATEMESIS may occur
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Diagnostic Evaluation
1) Upright chest X-ray may reveal a retrocardiac
shadow or widening
Paraesophageal HH:
1) Air fluid level behind the heart
2) Nasogastric tube that appears o enter the abdomen
but then curves back to the chest
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A plain chest radiograph showing a well-defined, rounded,
soft-tissue mass in the retrocardiac region consistent with a
sliding hiatal hernia55
A frontal chest radiograph in a patient with a large hiatal
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A frontal chest radiograph in a patient with a large hiatal
hernia demonstrating a retrocardiac opacity with radiolucent
gas, which shifts the mediastinum to the right
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A lateral chest radiograph showing a hiatal hernia.
Note the absence of fundal gas below the left
hemidiaphragm57
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2) Barium Swallow/upper GI series: usually diagnostic
to differentiate the type of HH & may rule out other
pathology
A barium-meal
examination in a
patient with a
sliding hiatal
hernia that
demonstratessupradiaphragma
tic location of the
gastroesophagea
l junction
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3) Upper GI endoscopy: allow direct visualization of
the hernia and evaluation of the esophageal and
gastric mucosa
4) Chest and abdominal CT Scan are often diagnostic
& provide excellent anatomic information.
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Treatment/ManagementSliding Hernias Paraesophageal Hernia
1) Rarely require treatment
2) If reflux (+), the treatment is
directed at correcting the
reflux disease (lifestyle
modifications: weight loss,dietary changes, avoidance
alcohol & tabacco,
avoidance of food within 4
hours of bedtime & sleeping
with head elevated & anti-
ulcer/antacid)
1) Always operative, regardless
of severity of symptoms, due
to the risk of gastric
VOLVULUS &
INCARCERATION.2) Surgical treatment: reducing
of the stomach into the
abdominal cavity, repairing
the esophageal hiatus, and
possibly an anti-reflux
procedure
3) Gastropexy
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Prognosis/Complication
Infarction, bleeding & perforation may occur in up
to 25% of patients with PEH
Elective surgical repair of PEH carries low operative
mortality
Emergency repair for infarction/perforation of the
stomach carries nearly 20% operative mortality
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Which one is true about Hiatus Hernia?
a) Is an uncommon finding
b) Is caused by stomach herniating through the
membranes part of the diaphragm
c) The rolling type is more commonly associated with
reflux
d) The rolling or paraesophageal type is best
managed conservativelye) Often co-exists with diverticular disease and gall
stones
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OESOPHAGEALCARCINOMA
By: Hidayah
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Malignancy of the esophagus. There are various subtypes,primarily adenocarcinoma (approx. 50-80% of allesophageal cancer) and squamous cell cancer
Most esophageal cancers fall into one of 2 classes:
a) SCC
similar to head & neck cancer in their appearance &association with tobacco/alcohol consumption
b)adenocarcinomas
often associated with a history of GERD and Barrett'sesophagus.
A general rule of thumb is that a cancer in the upper two-thirds is a squamous cell carcinoma and one in the lowerone-third is a adenocarcinoma.
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Clinical features
Dysphagia : first symptom in most patients. Fluids andsoft foods are usually tolerated, while hard or bulkysubstances (such as bread or meat) cause much moredifficulty
Odynophagia Weight loss: as a result of poor nutrition and the
active cancer
Pain : often of a burning nature, may be severe and
worsened by swallowing, and can be spasmodic incharacter. An early sign may be an unusually husky orraspy voice.
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Aspiration pneumonia: Disrupt normal peristalsis (the
organised swallowing reflex), leading to nausea and
vomiting, regurgitation of food, coughing and an
increased the risk.
Hematemesis : the tumor surface may be fragile and
bleed.
Compression of local structures occurs in advanceddisease, leading to such problems as upper airway
obstruction and superior vena cava syndrome.
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Fistulas may develop between the esophagus and
the trachea, increasing the pneumonia risk; this
condition is usually heralded by cough, fever or
aspiration.
If the disease has spread elsewhere, this may lead
to symptoms related to this: liver metastasis could
cause jaundice and ascites, lung metastasis couldcause shortness of breath, pleural effusions etc.
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Causes (Increased Risk)
Age. Most patients are >60, and the median in USpatients is 67.
Sex. (>men)
Heredity.
Tobacco smoking and heavy alcohol use & togetherappear to increase the risk >either individually.
GERD and its resultant Barrett's esophagus increaseesophageal cancer risk due to the chronic irritation of themucosal lining (adenocarcinoma is >common in thiscondition, while all other risk factors predispose more forSCC).
Human papillomavirus (HPV)
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Corrosive injury to esophagus by swallowing strongalkalines (lye) or acids.
Particular dietary substances, such as nitrosamine.
A medical history of other head and neck cancersincreases the chance of developing a second cancerin the head and neck area, including esophagealcancer.
Plummer-Vinson syndrome (anemia and esophagealwebbing)
Tylosis and Howel-Evans syndrome (hereditarythickening of the skin of the palms and soles).
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Radiation therapy for other conditions in themediastinum
Coeliac diseasepredisposes towards squamous cell
carcinoma. Obesity increases the risk of adenocarcinoma fourfold.It
is suspected that increased risk of reflux may be behindthis association.
Drinking hot brewed tea Alcohol consumption in individuals predisposed to
alcohol flush reaction
Achalasia
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Diagnostic Evaluation
Hx & PE:
evaluate degree of dysphagia (e.g.,solids vs liquids)
subjective location of swallowing dificulty (cervical
esophagus/thoracic esophagus/distal esophagus), presence of lymphadenopathy/abdominal
mass/hepatomegaly
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Upper GI endoscopy with biopsy is diagnostic
Barium esophagogram
CT, broncoscopy & endoscopic ultrasound (mostaccurate) are used for staging and to evaluate formetastases and local invasion.
Additional exaluation may include a FNA ofmetastatic lesions.
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Treatment/Management
Tx: primarily palliative
Surgical resection is rarely curative but may restore
patency of the esophagus
Total esophagectomy for SCC (with reconstruction usingeither the stomach or colon)
Esophagogastrectomy for Adenocarcinoma
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Esophageal dilation/stenting is indicated for
patients with esophageal obstruction or
tracheoesophageal fistula
Radiation @ chemotherapy may marginally improve
survival and/or temporarily relieve dysphagia
Laser & photodynamic therapy
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Prognosis/Complications
Poor Prognosis:
o SCC: 5-year survival
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Which of the following statements relating
to esophageal cancer is incorrect?
a) Is usually diagnosed at an early stage
b) Risk factors include smoking and alcohol
c) Treatment may include radiotherapy &
chemotherapy
d) Is predominantly adenocarcinoma in the UK
e) Dysphagia and weight loss are poor prognostic
signs
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Oesophageal Diverticula
Abnormal protrusions from the oesophagus that in
rare cases cause dysphagia and regurgitation
associated with motility disorders of the esophagus,
such as esophageal spasm and achalasia
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Oesophageal Diverticula
Zenker's Diverticula
A.k.a pharyngeal pouch
caused by an incoordination between movement of
food out of the mouth and relaxation of thecricopharyngeal muscle
This diverticulum can filled with food regurgitatedwhen the person bends over or lies down.
Regurgitate during sleep resulting in aspiration
pneumonia. Rarely, the pouch enlarges and causes swallowing
difficulty and sometimes a swelling in the neck.
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Midesophageal Diverticula
A midesophageal pouch or traction diverticulum is
caused by:
traction from inflamed lesions located in the chest outside theesophagus (mediastinum) or,
secondarily, by esophageal movement (motility) disorders.
A traction diverticulum rarely causes symptoms, but the
underlying disorder may.
Oesophageal Diverticula79
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Oesophageal Diverticula
Epiphrenic Diverticula:
An epiphrenic pouch or diverticulum occurs just above
the diaphragm and usually accompanies a motility
disorder (such as achalasia or esophageal spasm). An epiphrenic diverticulum rarely causes symptoms, but
the underlying disorder may.
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81
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PLUMMER VINSONSYNDROME
By: Nubla
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Plummer Vinson Syndrome
Usually occur in middle aged women
Clinical features: dysphagia, signs of anemia
(kiolonychia, smooth tongue, angular stomatitis)
Triad: oesophageal web, mucosal lesions of mouth
and parynx, iron deficiency anemia
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Investigations
Full blood count: hypochromic microcytic anemia,
low serum ferritin levels
Barium swallow: narrowing of the upper
esophagus with a web in the anterior wall Endoscopy: friable web can be seen across the
lumen of the esophagus
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