Dysphagia

Cam Edit

Ian Paul Titus DM FRCS

 Patient complains of”:
• “Food sticks” in upper or lower chest
• Food/liquids “come back up on me”
• Often no smell ( ie. not vomitus)
• Discomfort is common
• Pain is a bad sign

• DIFFERENT PATTERNS OF
DYSPHAGIA
 DYSPHAGIA FOR SOLIDS
• Implies a FIXED, inelastic, obstruction
– Eg. Foreign Body (esp. in children)
– Stricture (fibrous, benign)
 Caustic (lye, bleach, acid)

MALIGNANCY ( CA OESOPHAGUS)
 Mechanism of Dysphagia for
Solids:
• Rigid obstruction
• Solids cannot induce receptive relaxation
due to fibrous tissue or tumour tissue
• Liquids can “seep” past the obstruction

Therefore, the patient has more trouble

swallowing solids than liquids, initially
 Dysphagia for Liquids > Solids
• Typically, due to a NEUROLOGICAL
DISORDER OF THE OESOPHAGUS
 ACHALASIA
 CHAGAS’ DISEASE (parasitic
secondary achalasia)

• MYENTERIC PLEXUS is responsible for

inducing relaxation of the the usually tonically
contracted oesophageal circular muscle
 Mechanism of Dysphagia for
Liquids > Solids
• Loss of neurons in Myenteric Plexus results
in LOSS OF RELAXATION of the
denervated segment of the gullet

• Solids can “force relaxation” via

gravitational effects, while liquids are less
efficient at doing so
 Dysphagia

Nutcracker
esophagus
 Dysphagia
• Related to phases of swallowing:
– ORAL
• Functional and Mechanical
– PHARYNGEAL
• Functional and Mechanical
– ESOPHAGUS
• Functional and Mechanical

• Will discuss:
• Gastroesophageal Reflux Disease
• Achalasia
• Motility Disorders
• Carcinoma of the Oesophagus
 G.E.R.D.

• Reflux of gastric contents into the

Oesophagus, which may be symptomatic or
asymptomatic and is caused by a variety of
anatomic and physiological abnormalities.
 G.E.R.D.

• Symptoms may be classified thus :

• Typical
– Heartburn
– Regurgitation
– Dysphagia
– Water brash

• Atypical
– Pulmonary aspiration
– Chest pain
– Pulmonary asthma
– Chronic cough
– Choking
 G.E.R.D.
HIATUS HERNIA

• Type 1: Sliding hiatus hernia

– Abnormal position of GO junction
– Has no peritoneal sac
– Most are assymptomatic
– Type 1p indicates postoperative hernia
• Type 2: Para esophageal (rolling)
– Stomach herniates into the chest
– Has peritoneal sac
– Large herniation may cause volvulus
– May be assymptomatic
– Type 2p indicates postoperative hernia
• Type 3: Combined Type 1 & 2
– Type 3p indicates postoperative hernia
 G.E.R.D.
HIATUS HERNIA

• Only 50% of patients with GERD have HH

• More than 30% of patient with HH have no GERD
• Severe types of HH tend to produce more symptoms
• The anatomic and physiological GO sphincter is important
• Other factors play a role in reflux causation
 G.E.R.D.
HIATUS HERNIA

• Anatomic sling
• Oesophageal muscle
• Gastric muscle
• Diaphragm
 G.E.R.D.
Predisposing Factors

• Increased Gastric Acid Secretion

• Incompetent L.O.S.
• Delayed gastric emptying.
• Drugs e.g. hormones, NSAID
• Smoking and alcohol
• Pregnancy and weight increase
• Obesity
• Physical factors e.g. bending, straining, supine
• Disruption of mucosal defenses.
 G.E.R.D.
Patient Evaluation

• History & physical examination

• Establishes presence of typical or atypical symptoms
• Prepares a differential diagnosis
• Other causes of Dysphagia
• Dyspepsia and its causes
• Myocardial disease

• Treatment of symptoms
• Investigations
 G.E.R.D

Early
Symptomatic
Treatment
Flowchart
 G.E.R.D
Investigations

• To detect structural abnormalities

• Barium swallow meal and follow through.
• Endoscopy
• To detect functional abnormalities
• Stationary manometry
• 24 hr ambulatory manometry
• Video/cineradiography
• To detect increase exposure to gastric juice
• pH monitoring
• Standard acid reflux test (SART)
 G.E.R.D
Radiography

• Barium swallow meal and follow through.

– Rules out other causes of Dysphagia
– Small hiatus hernia are insignificant
– Large hernia may be demonstrated.
– Usually is not diagnostic in patients with mild
to moderate symptoms
 G.E.R.D
Endoscopy

• Not mandatory in all patients.

• May be normal.
• Documents mucosal disease.
• Inflammation & ulceration
• Locates the squamocolumnar junction.
• Inflammation usually contiguous with SC junction.
• Evaluates metaplasia
• Detects hiatus hernia.
• Evaluates strictures
• Allows Biopsy
 G.E.R.D
Endoscopy

Single isolated lesion

Circumferential lesions
 G.E.R.D
Endoscopy

Chronic lesions with

fibrosis

Columnar epithelium
(Barrett's Oesophagus)
 G.E.R.D
Treatment

• Lifestyle Modification
• Medical : Drugs
• Surgery
 G.E.R.D.
Lifestyle Factors
• Diet
– Chocolate, peppermint, raw onions, fats, lower LOS pressure
– Coffee, cola, beer, increase gastric secretion
– Coffee and citrus are direct irritants
– Avoid meals 3Hrs prior to going to bed
• Posture
– Elevate head of bed, sleep on pillows.
– Avoid straining, heavy lifting.
• Smoking & alcohol
Weight loss
– Improves symptoms but may be due to dietary change
• Medications
– Theophilline, Ca.channel blockers, NSIADS
 G.E.R.D.
Drug Therapy

• Antacids
– Relieves symptoms, poor healing of lesions.
• H2RA
– Ranitidine, Famotidine, Nizatidine
– 50 – 70% healing in mild to moderate disease
• PPI’s
– Omeprazole Lansoprazole
– > 80% healing in mild to moderate disease
– > 50% healing in severe disease
• Prokinetic Agents
– Cisapride Metoclopramide.
 G.E.R.D.
Surgery

• Indications
• Repeated failure of medical therapy
• Complicated disease
• Persistent reflux
• Stricture
• Metaplasia
• Again becoming popular due to
laparoscopic technique
• Endoscopic (Stretta procedure)
 G.E.R.D.
Surgery

• Should restore competence of cardia.

• Should treat any hiatus hernia
• Should restore oesophageal length
• Should not cause obstruction
• Requires some form of fundoplication.
 G.E.R.D.
Surgery

o
• Nissen : 360 fundoplication.
o
• Belsey Mark IV : 270 fundoplication
• Hill gastropexy : imbrication of ant and post
walls of fundus around oesophagus
• Collis gastroplasty.
• Stretta procedure : radio frequency energy
to the GO junction via electrodes.
 ACHALASIA

• An oesophageal motility disorder

characterized by absence of oesophageal
peristalsis and failure of the lower
oesophageal sphincter to relax during
swallowing.
• Receptive relaxation propels the bolus
down – denervation causes tonicity
 ACHALASIA
Pathogenesis

• Happens over a long period of time

• Primary degeneration of peripheral neurons.
• Primary degeneration of central neurons.
• Autoimmunity (Class II HCA DQw1).
• Neurotrophic infectious agents.
 ACHALASIA
Clinical Features

• Incidence of 0.4 to 0.6 / 100,000 (about 1 per 100,000)

• Any age but majority between 20 to 40 yrs.
– In the elderly, one must consider pseudoachalasia which would
signify malignancy
• Male = female.
• Variable degree of liquid dysphagia.
• 60 – 90% have regurgitation which may lead to
microaspirations and nocturnal asthma
• 30 – 50% have chest pain.
• Weight loss is a good indicator of severity.
• 5% of patients develop carcinoma at 20 yrs.
– Chronic irritation due to retained food in the esophagus
 ACHALASIA
Diagnosis

• Barium swallow shows proximally

dilated oesophagus.
• Varying degrees of tortuosity.
– GRADES I - IV
• “Bird beak or rat tail” entrance into
stomach.
• Smooth wall to oesophagus with
minimal peristalsis.
• Air-fluid level in oesophagus.
• Absence of gastric bubble.
 ACHALASIA
Diagnosis
• Plain Chest X-ray
– Air-fluid level in the mediastinum
• Endoscopy : dilated patulous oesophageal body.
– Rules out cancer
– May notice increased LES tone
– Mucosae is ulcerated and friable due to chronic irritation.
• Manometry demonstrates absent peristalsis.
• LOS pressures elevated > 50 mm Hg are diagnostic.
Proximal pressure usually 10 – 20mmHg.
– Incomplete relaxation of LOS.
• Oesophageal pH testing
– Rule out GERD which would have acidic pH
– Achalasia would have alkaline pH due to saliva in retained
food bolus
 ACHALASIA
TREATMENT: Risk of cancer is only decreased after treatment

CONSERVATIVE
• Endoscopic Oesophageal Dilatation
http://www.bing.com/videos/search?q=Esophageal+dilatation+&view=detail&mid=BA2151F4F1A6A6BAE85BBA2151F4F1A6A6BAE85B&first=0

– Mercury-filled bougie
– Pneumatic Balloon
• Relaxation by injection – repeated every
3 – 4 months
– BOTULINUM: Inhibits Ach release at presynaptic
nerves
– Ca2+ CHANNEL BLOCKERS: works better with
esophageal spasm
 ACHALASIA
TREATMENT: Risk of cancer is only decreased after treatment

SURGICAL
• Open Surgery
– Heller’s Cardiomyotomy + Antireflux
procedure (Nissen fundoplication; 2700 fundoplication
prefered; 1800 wrap may be done – put a large dilator [50F]
before doing wrap to ensure the wrap is loose enough)
• lasts for 30+ years
• COMPLICATIONS: strictures; usually does not represent with re-achalasia
• If no antireflux procedure, put the patient on proton pump inhibitors for long-
term use. Otherwise, a strictue will develop.
– Laparotomy
– Thoracotomy
• Laparoscopic surgery
 Motility Disorders
Diffuse Oesophageal Spasm

• Substernal pain more than achalasia.

• Dysphagia less than achalasia.
• 5 times less common as achalasia.
• Affects the body of the oesophagus.
• Rapid progression of contractions
downwards.
• Manometry shows frequent repetitive
high amplitude contractions.
• There may be muscle hypertrophy and
diverticulae.
• Treated by Transthoracic Myotomy
 Carcinoma of the Oesophagus

• Abnormal proliferation of cells in the mucosa of the esophagus

characterized by abnormal mitoses, pleomorphic cells and
dysfunctional apoptosis.

• 3 – 5/ 100,000 in Jamaica and areas of low incidence

– In Jamaica, highest incidence is in Spaldings and is thought to be
connected to CADMIUM in the soil
– Low risk areas include Trelawney, St. James and Portland
– Notably, patients who change areas still have the same risk. GENETIC?
EARLY ENVIRONMENT?
• 20/100,000 in the United States and areas of intermediate
incidence
• 100/100,000 in South Africa and other areas of high incidence
 Carcinoma of the Oesophagus
• Associated with:
– Cigarette smoking especially those who concomittantly
drink alcohol SQUAMOUS CELL CA
– Alcohol intake
– Nitroso compounds
– Vitamin A, C, E, B12 & Folic acid deficiency.

• Usually squamous cell but adenocarcinoma increasing

• Barrett’s Oesophagus predisposes to adenocarcinoma.

 Carcinoma of the Oesophagus
• TYPES
– Squamous cell: upper third (20%) and middle
third (50%) MOST COMMON

– Adenocarcinoma: lower third (30%)

BECOMING MORE COMMON due to
Barrett’s Esophagus
 Carcinoma of the Oesophagus

• Affects the elderly > 60yrs.

• Male > Female at 5:1
• Usually presents with anorexia &
weight loss.
• Dysphagia usually presents late.
• Extension of tumour causes:
– Stridor
– Tracheoesophageal fistula
– Erosion of aorta or pulmonary vessels.
– Vocal cord paralysis
• Metastases to liver bone and lung.
 Carcinoma of the Oesophagus
CLINICAL PRESENTATION:
• Dysphagia
– Progressive for solids before liquids and total dysphagia
– Usually painless

• Chest pain
– Radiating to the back

• Aspiration pneumonia/ pneumonia secondary to

fistula formation
– Upper and middle third of the esophagus

• Weight loss
– Due to cancer
– Due to poor nutrition
 Carcinoma of the Oesophagus
CLINICAL PRESENTATION:

• Loss of appetite
– Even after surgery
– Secondary to cancer
– Secondary to depression because patient is not able to get food down

• Hoarseness
– Infiltration of the recurrent laryngeal nerve in the tracheoesophageal
groove

• Food-sticking
– Patient knows the exact point where the food sticks
 Carcinoma of the Oesophagus

• Barium swallow and meal

– Mild or no proximal dilatation as the
history usually lasts months (c.f. achalasia)
so not enough time for esophagus to dilate.
There is also thickening of the wall adjacent to
the carcinoma
– Shouldering
– Mucosal irregularity
– Fissuring
– Fistula formation
 Carcinoma of the Oesophagus
• Chest X-ray/ CT Chest and Abdomen
– Metastasis is usually due to direct spread but hematogenous and lymphatic
spread can occur
– May see increased soft tissue density

• Endoscopy (awake; conscious sedation; turn scope 180 degrees to view

the GE Junction) / Rigid esophagoscopy (general anaesthesia:

45cm long) + Biopsy

• Endoscopic ultrasound allows accurate

staging – especially in early lesions
– Depth of tumour and lymph node involvement determines prognosis

• Bronchoscopy for mid-oesophageal lesions

 Carcinoma of the Oesophagus

• Chest X-ray important in evaluation.

• Patients should have lung function tests.
• Respiratory complications significant post-op.
• E.C.G. as most patients are > 50 yrs.
• Patients with ascites are poor surgical risks.
Carcinoma of the Oesophagus
T.N.M. Staging
 Carcinoma of the Oesophagus
Treatment Options

Mainly Surgical
• Curative resection
• Palliative resection or bypass
Non-surgical
• Oesophageal dilatation, intubation, stenting,
ablation and cryotherapy
• Radiotherapy – not a candidate for resection
• Chemotherapy – not efficacious/ increases
survival in 5 – 10%
 SURGICAL OPTIONS
• Resection (palliative or curative)
– Esophageal length must be preserved
– Segment must be replaced
• Colon – mobile blood supply
• Small intestine – less common as blood supply not
as mobile. The mesentery is long enough for
transposition. Anastamose the blood supply with the
internal mammary or veins.
• Stomach – MOST COMMON as it has a rich blood
supply. The blood vessels along the surface are
removed and the stomach is pulled up into the chest
as far as the neck
 SURGICAL OPTIONS
• Resection (palliative or curative)

MULTIPLE INCISIONS
One must ALWAYS be in the abdomen to free up the stomach

1. IVER-LEWIS OPERATION
- midline upper laparotomy to free up the stomach
- right thoracotomy to resect the esophagus
2. THREE INCISION OPERATION
 SURGICAL OPTIONS
• Bypass
– The stomach or colon may be used
– Patient does not do well
• 12% mortality rate due to poor clinical state at
operation
 RESECTABILITY
• Resectability and fitness for surgery
assessed by:
– Chest x-ray
– Lung function tests(FEV1 > 1L)
– Liver ultrasound
– Endoscopic ultrasound
– Bronchoscopy
– Laparoscopy
– Thoracic CT
 SURGICAL PALLIATION
• Open Gastrostomy/ Jejunostomy
– Tube feeding is a last resort
– It may also be used as bridging therapy. It is
not DEFINITIVE management
– Patients do poorly because they want to be able
to swallow
– Jejunostomy is preferred because it preserves
the stomach for surgery and aids in nutrition
 NON-SURGICAL OPTIONS
• Dilatation
– Not long term and does not last long
– Done in patients with advanced disease who need palliation for swallowing

• Intubation – useful when there is a fistula

– Mousseau Barbin Tube: Rubber, needs Laparotomy
– HISTORICAL SIGNIFICANCE: Endoscopic or radiological
placement now most commonly practiced

• Esophagoscopy and Stenting

– A guide wire is placed into the stomach
– Stent is placed via traction technique from below then released into the
esophagus
• Self-expandable
• Rigid plastic
– Advantageous because the patient can be fed immediately unlike surgery where
the patient has to wait 3 – 5 days
Complications of NON-SURGICAL
METHODS
• Complications of stents and tubes:
– Oesophageal perforation
– Tube displacement or migration
– Tube blockage due to ingrowth or overgrowth
 NON-SURGICAL OPTIONS
• Ablation
– There is an increased risk of perforation. The aorta may
even be perforated
– Laser
– Phototherapy
• A photosensitive liquid is placed in the cancer cells and they
explode

• Cryotherapy
– Limited use
 NON-SURGICAL
PALLIATION
• Percutaneous Endoscopic Gastrostomy
(PEG tube)
– Usually done in patients with late presentation
as the scope cannot pass the mass
Carcinoma of the Oesophagus
Carcinoma of the Oesophagus
Chemotherapy

• CDDP
• Vinblastine
• 5 Flourouracil
• Bleomycin
 Treatment
• Fibrous Stricture
– Dilatation
– Surgical resection
 Treatment
• Malignant Stricture
– Dilatation
– Dilatation and RadioRx
– Resection
– Resection and RadioRx
– STENTING
– Bypass Surgery
– RadioRX (+/- chemoRx
– Gastrostomy/Jejunostomy