DYSPHAGIA

By
Dr Lawrence. A. Sereboe
Cardiothoracic Surgeon
KBTH
Accra
Definition

 A subjective awareness of difficulty in

swallowing caused by impaired progression
of matter from pharynx to stomach.
TYPES OF DYSPHAGIA

 PREOESOPHAGEAL DYSPHAGIA
 OESOPHAGEAL DYSPHAGIA
PREOESOPHAGEAL DYSPHAGIA
 Difficulty emptying bolus material from the
oropharynx into the oesophagus.
 Abnormal function proximal to the oesophagus
 Causes
 Myaesthenia gravis
 Muscular dysthrophy
 Bulbar poliomyelitis
 Pseudobulbar palsy
 Parkinson’s disease
OESOPHAGEAL DYSPHAGIA

 Difficulty passing food down the oesophagus.

 Causes
 Congenital
 Acquired
Oesophageal Dysphagia

 Causes
– Congenital
– Acquired
OESOPHAGEAL DYSPHAGIA

 Congenital causes
 Associated with oesophageal atresia/
tracheooesophageal fistula
 Webs
 Dysphagia lusoria
Oesophageal Dysphagia

 Causes
– Congenital
– Acquired
OESOPHAGEAL DYSPHAGIA

 Acquired
 Diseases of the wall of the oesophagus
 Intraluminal lesions
 Extrinsic pressure on the oesophagus
 Diseases of the stomach
Disease of the wall of the oesophagus

– Carcinoma of the oesophagus

– Benign tumours
– Oesophagitis/ stricture
 Corrosive burns ( acids, alkalis, various chemicals)
 Reflux oesophagitis
– Perforation
– Oesophageal diverticulae
– Neuromuscular dysfunction
 Achalasia cardia
 Diffuse spasm
– Connective tissue diseases
 Scleroderma
 SLE
 Polyarteritis nodosa
OESOPHAGEAL DYSPHAGIA

 Acquired
 Diseases of the wall of the oesophagus
 Intraluminal lesions
 Extrinsic pressure on the oesophagus
 Diseases of the stomach
Intraluminal Lesions

 Impacted foreign bodies

 Bolus obstruction e.g welle!
 Oesophageal web→ Plummer-Vinson
Syndrome
 Schatzki’s ring
OESOPHAGEAL DYSPHAGIA

 Acquired
 Diseases of the wall of the oesophagus
 Intraluminal lesions
 Extrinsic pressure on the oesophagus
 Diseases of the stomach
Extrinsic pressure on the oesophagus

 Goitre – neck or mediastinum

 Enlarged mediastinal lymph nodes
 Mediastinal tumours
 Aneurysm of ascending or arch of the aorta
OESOPHAGEAL DYSPHAGIA

 Acquired
 Diseases of the wall of the oesophagus
 Intraluminal lesions
 Extrinsic pressure on the oesophagus
 Diseases of the stomach
Diseases of the stomach

 Carcinoma of the cardia.

MANAGEMENT OF DYSPHAGIA

 History
 Physical examination
 Investigations
 Treatment
History

AGE
 Neonate -Congenital
 Child: -Foreign body
 Third or fourth decade: -Achalasia
 Elderly: -Carcinoma
History

 History of accidental or suicidal ingestion of

corrosive, or swallowing of a foreign body
 History of dyspepsia
 History of alcoholism/smoking
 Duration of Symptoms
Duration of symptoms

 Very short history suggests inflammatory or

traumatic lesion
 Long and intermittent – Achalasia
 Long and progressive – Stricture
 Short and progressive – Carcinoma
MANAGEMENT OF DYSPHAGIA

 History
 Physical examination
 Investigations
 Treatment
Physical examination

 Usually unhelpful
 Weight loss
 Anaemia
 Dehydration
 Peripheral lymph nodes
 Epigastric mass
MANAGEMENT OF DYSPHAGIA

 History
 Physical examination
 Investigations
 Treatment
Investigations
 Chest X-ray
 FB, Widened mediastinum, retrosternal or mediastinal
masses
 Barium swallow.
 Precedes oesophagoscopy- very important
 Oesophagoscopy
 identifies lesion and allows biopsy
 Manometry
 achalasia
 CT scan, MRI, USS
 Full Blood Count, BUE, LFTs, etc.
MANAGEMENT OF DYSPHAGIA

 History
 Physical examination
 Investigation
 Treatment
TREATMENT

 Depends on the diagnosis

ACHALASIA OF THE
CARDIA
DEFINITION

 Motility disorder of oesophagus of unknown

aetiology characterized by:
 Absence of peristalsis in the body of the oesophagus
 High resting pressure in the lower oesophageal
sphincter
 Inadequate or incomplete relaxation of the LES in
response to swallowing
 Hypertrophy and dilatation of the oesophagus
AETIOLOGY
 Cause is unknown
 Neurological basis
 Generally accepted
 Supported by absence/ or diminished ganglion cells of Auerbach’s
plexus.
 Vagus nerve dysfunction
 Indicated by abnormalities of gastric secretion, also supports
neurologic aetiology
 Similar clinical condition created in cats by destruction of the vagal
nuclei
 Chagas’ disease(Trypanosoma cruzi infection)
 In south America
 Show changes in Auerbach’s plexus indistinguishable from those of
Achalasia
AETIOLOGY

 Chagas Disease (Trypanosoma cruzi

infecton)
In South America
Produces lesions indistinguishable from
achalasia
Pathology

 Oesophageal obstruction at the gastro-

oesophageal junction with thickening and
tonic contraction of the sphincter
 Proximal oesophageal dilatation with
hypertrophy of the muscle layer
 Advanced cases show marked proximal
dilatation with food stasis and tortuosity of
the oesophagus
Clinical Features
 High incidence in patients btw 30- 60yrs
 M:F is 1:1
 Dysphagia with sticking sensation in the substernal
area
 Precipitated by an emotional disorder
 Odynophagia in 30% of patents, especially with cold
fluids
 Weight loss – long standing achalasia
 Malignant change ( middle of oesophagus)
Clinical Features

 Retrosternal Pain
 Regurgitation of food after meals and in late
stages during sleep
 Tracheobronchopulmonary soilage results in
recurrent bouts of bronchitis, pneumonia and
lung abscess.
 Weight loss-long standing achalasia
 Malignant change
Investigations

CXR: widened mediastinum with or without an

air fluid level
Absent gastric air bubble
Barium swallow with fluoroscopy: shows dilated
oesophagus, lack of peristalsis, retained food
in the oesophagus
Investigations

 Oesophagoscopy
Stasis, dilated oesophagus with retained food
oesophagitis
r/o carcinoma or other causes of stricture
 Manometric evaluation

-failure of relaxaton of the LES

-absent peristalsis in the body of the oesophagus
-elevated LES pressure
TREATMENT

 Aim is to relieve obstruction caused by the

hypertensive LES

 Medical
 Surgical
TREATMENT

 Medical – 50- 60 % satisfactory

 Dilatation of lower sphincter
 Mechanical
 Pneumatic- Stark dilator

 Hydrostatic- Negus hydrostatic bag

Complications: Perforation, gastro-oesophageal reflux

 Nitrates and calcium channel blockers. Results limited
by side effects
 Botulinum toxin
TREATMENT

 SURGICAL
– Heller’s oesophagocardiomyotomy
– Involves incision(8-12cm) through longitudinal and circular
muscle layers
– Mucus membrane pouches through the incision
 Abdominal approach
 Thoracic approach via left thoracoscopy
 Video Assisted thoracoscopy / laparoscopy
– Result of surgery - 80 – 95 % satisfactory
CORROSIVE OESOPHAGEAL
STRICTURES
CORROSIVE OESOPHAGITIS AND
STRICTURES

 AETIOLOGY
 PATHOLOGY
 CLINICAL FEATURES
 DIAGNOSIS
 TREATMENT
AETIOLOGY

 Ingestion of caustics
 Strong acids-sulphuric acid, hydrochlroric acid
phosphoric acid in battery acid, izal, DDT
 Alkalis-caustic soda
 Household bleaches, nail varnish
 Children
– Usually accidental
 Adults
– Accidental or suicidal
Pathology

 May Involve oropharynx, oesophagus,

stomach or jejunum
 Burns of exposed mucus membranes
 Degree of injury depends on the character
the concentration and pH of the corrosive
 Deep burns→ perforations
→mediastinitis/peritonitis
Pathology

 Alkalis cause liquefaction necrosis,

penetrates deeply into surrounding tissues
 Acids cause coagulation necrosis and less
penetration
 Healing with fibrosis results in stricture
Clinical features
 History of corrosive ingestion: accidental or
deliberate
 Dysphagia: spasm or inflammatory oedema or due to
stricture
 Burning pain in the mouth, throat and retrosternal
area
 Dyspnoea, stridor, wheezing, hoarseness due to
oedema of the tongue, pharynx and larynx
Clinical Features

 Shock and hypotension in severe cases

 Fever due to secondary infection,
mediastinitis or pneumonia
 Drooling of saliva
 Malnutrition, dehydration
Diagnosis

 Barium swallow
 Upper GI endoscopy

 Supportive investigations; FBC, BUE, LFTs,

CXR, etc.
Treatment

 Aimed at:
-Dilution and neutralizaton of the corrosive
agent
-Correction of shock
-Nutritional support
-Prevention of infection
Management of stricture
Treatment

 Early phase:
 Immediate dilution or neutralization with copious amount
of water, milk or beaten eggs. Magnesium tricilicate or
aluminium hydroxide for acids
 Analgesics: pethidine or morphine
 Parenteral fluids and alimentation
 Antibiotics
 Graded oral feeding
 Oesophagoscopy and dilatation
 ???steroids
Treatment

 Established stricture
 Dilatations
 Oesophageal replacement
 Colon
 Stomach
 Jejunum
 Oesophageal repair
 The Frimpong-Boateng sternomastoid pedicled flap
oesophagoplasty for short strictures of the cervical
oesophagus
CARCINOMA OF THE OESOPHAGUS
AETIOLOGY
 Not definitely known
 Endemic/ high prevalence areas
 China, Japan, Iran, Chile, Puerto Rico etc.
 Associated factors
 Age- 5th – 6th decade
 Dietary factors – alcohol, tobacco, malnutrition &
Nitrosamine
 Premalignant – Plummer-Vinson Syndrome, Barret’s
oesophagus, Lye burns of oesophagus
 Familial lesions – tylosis
PATHOLOGY

 Squamous cell Ca commonest ( >95%)

 Primary adenocarcinoma
 Adenocarcinoma in a Barret’s oesophagus
 Adenoid cystic Ca
 Mucoepidermoid Ca
Pathology

 Early lesion
 Erosive lesions
 Plaques
 Papillary
 Advanced lesion
 Fungating lesion
 Ulcerative lesion
 Infilterative lesion ( tend to produce malignant strictures)
Clincal features
 Progressive dysphagia
 From solid → semisolid → liquid and saliva
 Weight loss and weakness
 Regurgitation/ Aspiration/ Haematemesis/ Melaena
 Adjacent structure involvement
 Persistent back pain : paravertebral fascia
 Hoarseness & Dysphonia : Recurrent Laryngeal Nerve
 Hiccups : Phrenic nerve & diaphragm
 Respiratory difficulty: tracheal, bronchi
Investigations
 Diagnostic
 Barium swallow
 Oesophagoscopy + biopsy/ smear for cytology
 Chest x-ray
 CT scan of chest
 USS abdomen
 Supportive
 FBC
 BUE, Cr
 LFT’s
TREATMENT

 Depends on stage
 Early lesions
– Limited to oesophagus, no lymph node or metastasis
– Suitable for curative resection

 Advanced lesions
– Benefit from palliative treatment
TREATMENT

 Surgery
 curative
 palliative
 Chemotherapy
 Radiotherapy
 Oesophageal intubation
 Photodynamic therapy
TREATMENT

 Palliative surgery
– Bypass; stomach
 Gastric tubes

 Whole stomach

 Colon

 Resection + replacement/ bypass

 Endoprosthesis