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DYSPHAGIA
ByDr Lawrence. A. SereboeCardiothoracic SurgeonKBTHAccra
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