TBL 3: Dysphagia: By: Anis, Aishah, Nubla, Hanafi, Hidayah

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TBL 3:
DYSPHAGIA
By: Anis, Aishah, Nubla, Hanafi, Hidayah
 Dysphagia: is a difficulty in swallowing and always
need investigation to exclude malignancy.
 Odynophagia: is painfull while swallowing in the
mouth or oesophagus
 Globus hystericus :The sensation of having a lump
in the throat when there is nothing there
 If symptoms are progressive or prolonged then
urgent investigation is required.
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HOW TO TAKE
HISTORY?
Dysphagia
History
4
Physical Examination
5

Inspection
Mouth
 Ulcer

 Swelling -tonsil

 Hydration status

Neck
 Swelling or mass

 Lymph node
6

Abdominal examination
Respiratory examination
Causes of Dysphagia - Mural
7

Ca esophagus Progressive cause, LOW, anorexia, low-


grade anemia, small hematemesis
Reflux esophagitis Preceded by heartburn, progressive course,
& stricture nocturnal regurgitation
Achalasia Frequent regurgitation, recurrent chest
infection
Tracheo- Recurrent chest infection, coughing after
esophageal fistula drinking
Caustic stricture Examination shows corrosive ingestion,
chronic dysphagia
Scleroderma Slow onset, a/w skin and hair changes
Causes of Dysphagia - Intraluminal
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Foreign body Acute onset, marked retrosternal dicomfort,


dysphagia even to saliva
Causes of Dysphagia -
Extramural
Pulsion Intermittent symptoms, unexpected
diverticulum regurgitation
External Mediastinal lymph nodes, left arterial
compression hyperthrophy, bronchial malignancy
Risk Factors for Oesophageal Ca
9

Squamous cell carcinoma Adenocarcinoma


1. Heavy alcohol intake 1. Poor diet- low intake of
2. Smoker fruit and vegetables
3. Poor diet- low intake of 2. Acid suppressing
fruit and vegetables medications
3. Peptic oesophagitis and
stricture
4. Achalasia
5. Oesophageal web/
pharyngeal pouch
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INVESTIGATIONS
By: Aishah Azman
Investigations
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 Full blood count (FBC)


 Liver function test (LFT)
 Renal profile
 Chest Xray& CT scan
 Oesophageal-gastric-duodenal scopy (OGDS)
 Barium swallow
 Esophageal monometry
Full Blood Count
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 Anaemia – Tumours much more commonly cause


this rather than reflux
Test Result interpretation
Hemoglobin 10.4 Low
Hematocrit 31.1 Low
Mean Corpuscular 26. 2 Low
Hemoglobin
(MCH)
Platelets 595 High
RBC Dist Width 15.2 High
Total RBC 3.95 Low
Liver Function Test
13

 Looking out for any hepatic disease or involvement


Renal profile
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 To look for signs of dehydration

BUN 4.3 mmol/L N


Sodium 135.2 mmol/L N
Potassium 4.83 mmol/L N
Creatinine 89 Umol/L N
Chloride 103.7 mmol/L N
Chest X-ray and CT scan
15

 To rule out external compression


 Allow tumour staging
OGDS
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 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.
Barium Swallow
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 Patients with esophageal dysphagia often are evaluated first with a


radiographic barium study to differentiate between mechanical
lesions and motility disorders, providing important information
about the latter in particular.
 In patients with esophageal dysphagia and a suspected motility
disorder, 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
it better identifies mucosa lesions and permits mucosal biopsy and
dilation.
 However, barium study is more sensitive for detecting subtle
esophageal narrowing due to rings, achalasia, and proximal
esophageal lesions.
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Esophageal Monometry
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 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 a
diagnosis of achalasia is suspected by endoscopy or barium
study
 for the preoperative assessment of patients being
considered for antireflux surgery to exclude an alternative
diagnosis (eg, achalasia) or possibly to assess peristaltic
function in the esophageal body.
Investigations Gastro-esophageal Oesophagus ca Achalasia
reflux disease (GERD)
Barium swallow reverse flow of barium irregular, persistent, -uniformly dilated
into the lower end of intrinsic feeling defect oesophagus above,
oesophagus (from the with a smooth tapering
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stomach) segment below-
cucumber oesophagus
-chronic case, may be
sigmoid shape
Endoscopy red, angry looking -Early stage: superficial dilated sac containing
mucosa in the lower plaque or ulceration stagnant food & fluid
end of the oesophagus -Advance: ulcerated due to stasis which
mass with stricture or splashes out with each
circumferential mass heart beat & with each
or a large ulceration respiratory movement
Oesophageal - - -Hypertensive lower
manometry oesophageal sphincter
(LOS)
-increase resting
pressure in oesophagus
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ACHALASIA
By: Aishah Azman
Achalasia
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 The rhythmic contractions of the esophagus


are greatly decreased,  LES does not
relax normally, 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 a
hypertensive non-relaxed esophageal
sphincter.
Etiology/Pathophysiology
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 Most common 1° esophageal motility disorder


 Due to
 absence of esophageal smooth muscle peristalsis
 Increased lower esophageal sphincter (LES) resting
pressure
 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)
Achalasia vs other esophageal motility
disorders
24

 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
Signs and symptoms
25

 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 into
trachea
 Recurrent aspiration pneumonia
 Bloating
 Inability to burp
Diagnostic evaluation
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 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
Treatment and Management
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 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
Prognosis and Complication
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 Prognosis – increased risk of esophageal ca


 Pneumatic dilatation
 One: 60% effective
 Two: 80% effective
 Perforation: 2-15% (*increased with repeated dilatations and
prior botox)
 Botulinum injection
 40% : not effective
 Multiple injections
 Scar: increase risk of complication following pneumatid
dilatation or surgery
 Surgery – 3-4% : pneumothorax and esophageal mucosal
perforation
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 Oesophagitis
Symptomatic esophagitis occur with:
 Prolonged exposure of mucosa to excessive reflux,

both in number of episodes & volume.


 Impaired normal mechanisms from clearing the lower

esophagus.
 High levels of acid & pepsin.

 Presence of bile & pancreatic enzymes (alkaline

reflux).

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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 Barrett’s

oesophagus).
 Dysphagia from a benign stricture.

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Pathophysiology

35
36

 The action of the lower esophageal sphincter (LES) is


perhaps the most important factor (mechanism) for
preventing reflux.
 The esophagus is a muscular tube that extends from the
lower throat to the stomach. The LES is a specialized ring
of muscle that surrounds the lower-most end of the
esophagus where it joins the stomach. The muscle that
makes up the LES is active most of the time.
 This means that it is contracting and closing off the
passage from the esophagus into the stomach. This
closing of the passage prevents reflux. When food or
saliva is swallowed, the LES relaxes for a few seconds
to allow the food or saliva to pass from the esophagus into
the stomach, and then it closes again.
37

 Several different abnormalities of the LES have been found in


patients with GERD. Two of them involve the function of the
LES.
 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 swallows
and they last for a long time, up to several minutes. These
prolonged relaxations allow reflux to occur more easily.
 The transient LES relaxations occur in patients with GERD
most commonly after meals when the stomach is distended
with food. Transient LES relaxations also occur in individuals
without GERD, 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)
BARRET’S 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
lower esophagus decrease clearing & aggravate
reflux disease
4. Oesophageal shortening

39
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

40
3. Barret Oesophagitis
 Metaplastic change in the lining mucosa of the
oesophagus in response to chronic GORD
 Junction between squamousoesophageal mucosa and

gastric mucosa moves proximally


 Risk of adenocarcinoma (30 x)

 Divided into:

 Classic Barrett’s (3cm or more columnar epithelium)


 Short-segment Barret’s (less than 3cm)
 Cardiametaplasia (intestinal metaplasia at the
oesophagogastric junction without any macroscopic change
at endoscopy)
41
Causes & symptoms
 Barrett's esophagus is caused by GERD which
allows the stomach's contents to damage the cells
lining 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
45

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.
Barrett esophagus.

•Figure 17-6 Barrett esophagus. A, B, Gross view of distal esophagus (top) and proxim
stomach (bottom), showing A, the normal gastroesophageal junction (arrow) and C,
Endoscopic view of Barrett esophagus showing red velvety gastrointestinal mucosa
extending from the gastroesophageal orifice. Note the paler squamous esophageal muc

C, Endoscopic view
A, the normal gastro- B, the granular zone of showing red velvety
esophageal Barrett esophagus gastrointestinal mucosa
junction (arrow) (arrow). extending from the
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gastroesophageal orifice.
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HIATUS HERNIA
By: Hidayah
Hiatal Hernia
48
49
Hiatus Hernia
50

 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
Sliding HH PEH

51
(90% of cases): upward is a rolling of the gastric
migration of the GEJ fundus upward through the
through the esophageal esophageal hiatus into the
hiatus and into the thorax esophageal hiatus and ino
the thorax, with normal
Most often caused by position of the GEJ
strecthing the esophageal
hiatus It have a significantly
increased risk of
VOLVULUS &
STRANGULATION
 Classification

52
Clinical features
53
Diagnostic Evaluation
54

 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
A plain chest radiograph showing a well-defined, rounded,
soft-tissue mass in the retrocardiac region consistent with
a sliding hiatal hernia
55
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
56
A lateral chest radiograph showing a hiatal hernia.
Note the absence of fundal gas below the left
57 hemidiaphragm
2) Barium Swallow/upper GI series: usually
diagnostic to differentiate the type of HH & may
58 rule out other pathology

A barium-meal
examination in a
patient with a
sliding hiatal
hernia that
demonstrates
supradiaphragma
tic location of the
gastroesophagea
l junction
59

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.
Treatment/Management
Sliding Hernias Paraesophageal Hernia
60

1) Rarely require treatment 1) Always operative, regardless


2) If reflux (+), the treatment is of severity of symptoms, due
directed at correcting the to the risk of gastric
reflux disease (lifestyle VOLVULUS &
modifications: weight loss, INCARCERATION.
dietary changes, avoidance 2) Surgical treatment: reducing
alcohol & tabacco, of the stomach into the
avoidance of food within 4 abdominal cavity, repairing
hours of bedtime & sleeping the esophageal hiatus, and
with head elevated & anti- possibly an anti-reflux
ulcer/antacid) procedure
3) Gastropexy
Prognosis/Complication
61

 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
Which one is true about Hiatus
62
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 conservatively
e) Often co-exists with diverticular disease and gall
stones
63

OESOPHAGEAL
CARCINOMA
By: Hidayah
64

 Malignancy of the esophagus. There are various


subtypes, primarily adenocarcinoma (approx. 50-80% of
all esophageal 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's
esophagus.
 A general rule of thumb is that a cancer in the upper two-
thirds is a squamous cell carcinoma and one in the lower
one-third is a adenocarcinoma.
Clinical features
65

 Dysphagia : first symptom in most patients. Fluids


and soft foods are usually tolerated, while hard or
bulky substances (such as bread or meat) cause much
more difficulty
 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 in
character. An early sign may be an unusually husky
or raspy voice.
66

 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 advanced
disease, leading to such problems as upper airway
obstruction and superior vena cava syndrome.
67

 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 could
cause shortness of breath, pleural effusions etc.
Causes (Increased Risk)
68

 Age. Most patients are >60, and the median in US


patients is 67.
 Sex. (>men)
 Heredity.
 Tobacco smoking and heavy alcohol use & together
appear to increase the risk >either individually.
 GERD and its resultant Barrett's esophagus increase
esophageal cancer risk due to the chronic irritation of the
mucosal lining (adenocarcinoma is >common in this
condition, while all other risk factors predispose more for
SCC).
 Human papillomavirus (HPV)
69

 Corrosive injury to esophagus by swallowing strong


alkalines (lye) or acids.
 Particular dietary substances, such as nitrosamine.
 A medical history of other head and neck cancers
increases the chance of developing a second cancer
in the head and neck area, including esophageal
cancer.
 Plummer-Vinson syndrome (anemia and esophageal
webbing)
 Tylosis and Howel-Evans syndrome (hereditary
thickening of the skin of the palms and soles).
70

 Radiation therapy for other conditions in the


mediastinum
 Coeliac diseasepredisposes towards squamous cell
carcinoma.
 Obesity increases the risk of adenocarcinoma
fourfold.It is suspected that increased risk of reflux may
be behind this association.
 Drinking hot brewed tea
 Alcohol consumption in individuals predisposed to
alcohol flush reaction
 Achalasia
Diagnostic Evaluation
71

 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
72

 Upper GI endoscopy with biopsy is diagnostic

 Barium esophagogram

 CT, broncoscopy & endoscopic ultrasound (most


accurate) are used for staging and to evaluate for
metastases and local invasion.

 Additional exaluation may include a FNA of


metastatic lesions.
Treatment/Management
73

 Tx: primarily palliative


 Surgical resection is rarely curative but may restore
patency of the esophagus
 Total esophagectomy for SCC (with reconstruction
using either the stomach or colon)
 Esophagogastrectomy for Adenocarcinoma
74

 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


Prognosis/Complications
75

 Poor Prognosis:
o SCC: 5-year survival <10%
o Adenocarcinoma: 5-year survival <5%

 75% of patients have cervical @ supraclavicular


nodal involvement at time of presentation.
Which of the following statements relating
to esophageal cancer is incorrect?
76

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
Oesophageal Diverticula
77

 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
Oesophageal Diverticula
78

• Zenker's Diverticula
– A.k.a pharyngeal pouch
– caused by an incoordination between movement of
food out of the mouth and relaxation of the
cricopharyngeal muscle
– This diverticulum can filled with food  regurgitated
when 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.
Oesophageal Diverticula
79

 Midesophageal Diverticula
 A midesophageal pouch or traction diverticulum is
caused by:
 traction from inflamed lesions located in the chest outside
the esophagus (mediastinum) or,
 secondarily, by esophageal movement (motility) disorders.
 A traction diverticulum rarely causes symptoms, but
the underlying disorder may.
Oesophageal Diverticula
80

 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.
81
82

PLUMMER VINSON
SYNDROME
By: Nubla
Plummer Vinson Syndrome
83

 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
Investigations
84

 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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