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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