copy of dysphagia lecture notes

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


Congenital causes Associated with oesophageal atresia/

tracheooesophageal fistula Webs Dysphagia lusoria

Oesophageal Dysphagia

Causes– Congenital – Acquired


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

Intraluminal Lesions

Impacted foreign bodies Bolus obstruction e.g welle! Oesophageal web→ Plummer-Vinson

Syndrome Schatzki’s ring

Extrinsic pressure on the oesophagus

Goitre – neck or mediastinum Enlarged mediastinal lymph nodes Mediastinal tumours Aneurysm of ascending or arch of the aorta

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

Physical examination

Usually unhelpful Weight loss Anaemia Dehydration Peripheral lymph nodes Epigastric mass

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.


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

copy of dysphagia lecture notes

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