Transcript Surgical issues of the Oesophagus

Surgical issues of the
Oesophagus
Dr. S. Nishan Silva
( MBBS )
Oesophagus – Normal Anatomy
• Extends from Pharynx (C6) to Gastro oesophageal
junction (T11/T12)
• 25.0 cm in length.
• 3 points of narrowing Cricoid cartilage
L/S Bronchus
Diaphragm.
• UES – 3cm segment at the cricopharyngeal muscle.
• LES – 2 – 4 cm segment in the abdomen proximal to
the anatomical GE sphincter.
Esophageal Anatomy
Upper Esophageal
Sphincter (UES)
Esophageal Body
(cervical & thoracic)
Lower Esophageal
Sphincter (LES)
18 to 24 cm
Oesophagus - Histology
• Mucosa – non keratinizing
squamous epithelium.
• Submucosa – loose
Connective tissue.
• Muscularis propria
– Inner – circular
– Outer – Longitudinal
Skeletal mm fibres in the
initial 10 – 12 cms.
(Cricopharngeus)
• Serosal Coat - ABSENT
Normal Swallowing
Frontal cortex
Cortical Swallowing Areas
Swallowing Center
Brainstem
Motor Nuclei
Oropharynx & Esophagus
Symptoms of dysphagia
Esophageal dysphagia
Sensation of food sticking in the chest
Oral or pharyngeal regurgitation
Food sticking in the throat
Drooling
Unexplained weight loss
Change in dietary habits
Recurrent pneumonia
Causes of dysphagia
• Neurologic disorders and stroke
Cerebral infarction
Brain-stem infarction
Intracranial hemorrhage
Parkinson's disease
Multiple sclerosis
Amyotrophic lateral sclerosis
Poliomyelitis
Myasthenia gravis
DementiasPsychiatric disorder
Psychogenic dysphagia
Causes of dysphagia
• Structural lesions
Thyromegaly
Cervical hyperostosis
Congenital web
Zenker's diverticulum
Ingestion of caustic material
Neoplasm
Causes of dysphagia
• Connective tissue diseases
Polymyositis
Muscular dystrophy
• Iatrogenic causes
Surgical resection
Radiation fibrosis
Medications
Oesophageal disorders
• Congenital abnormalities
• Motility disorders
– Achalasia cardia
– Oesophageal diverticula
– Rings and webs
• Ulcerations and lacerations
• Vascular lesions
• Organic lesions
– Strictures and tumours
Congenital abnormalities – Tracheo
oesophageal fistula
Commonest is
Type C
Congenital abnormalities
• Stenosis
• Atresia
• Heterotopia – Gastric mucosa
Sebaceous glands.
• Cysts – Inclusion cyst
– Columnnar and squamous epithelial lined cysts
Retention cysts.
Motility disorders
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Achalasia cardia
Diverticula
Rings and webs
Hiatus hernia *
Gastro oesophageal reflux disease *
Diverticula
Outpouchings of the the mucosa at points of weakness
PULSION DIVERTICULUM
Epiphrenic – above the
diagphragm
Zenkers – Pharyngo
oesophageal
TRACTION DIVERTICULUM
Pull due to attachement to
extrinsic structures
Eg: TB Lymph nodes
Diverticula
• MULTIPLE – Diffuse intramural oesophageal
diverticulosis.
• COMPLICATIONS – Obstruction, infection,
haemorrhage, perforation, increased incidence of
malignancy.
Achalasia Cardia
Achalasia cardia
• Failure of the cardia (LES) to open when the
peristaltic wave reaches it.
• Major abnormalities in the Achalasia cardia
Aperistalsis
Partial / complete relaxation of LES
Increased basal tone of LES
Achalasia cardia
• Symptoms – Progressive dysphagia.
Regurgitation of undigested food.
Aspiration pneumonia.
Retrosternal discomfort.
Foetid flatulence.
Achalasia cardia - Pathology
• Progressive dilatation of the upper segment
• Wall
– thickened proximally due to muscular hypertrophy.
– Wall thinned out due to dilatation.
– Normal in thickness
• Ganglia – absent in upper segment.
• Ulceration and inflammation of the oesophageal
lining.
Hiatus Hernia
Hiatus Hernia
• Sliding type – Disturbance of the normal
relationship of the gastro oesophageal
junction.
Reflux.
• Paraoesophageal / rolling type – Strangulation
& Obstruction.
Ulceration of the Oesophagus
• Mallory – Weiss Syndrome – ( laceration /
tear)
• Oesophagitis.
Mallory – Weiss Syndrome
• Tear in the
oesophageal mucosa
which is oriented
longitudinally astride
the oesophagogastric
junction: Common in
alcoholics.
Inflammations – Oesophagitis.
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Reflux oesophagitis.
Prolonged gastric intubation.
Ingestion of corrosive alkali, smoking.
Uraemia.
Bacteraemia / Viraemia. – HSV CMV,
Fungal infection – Candida, Mucor, Aspergillus.
Cytotoxic treatment.
Pemphigoid and Epidermolysis Bullosa.
Graft vs Host disease.
Relux oesophagitis (GERD/GORD)
• Reflux of gastric contents
• Inflammatory changes are due to
– Frequent protracted reflux - ? Incompentance of
the LES
– Disordered oesophageal motility – contact of
gastric contents with the oesophagus for longer
periods
– Elevated acid peptic levels in the gastric fluid
Barrett’s Oesophagus
• Congenital / Acqiured
(Reflux induced)
• Metaplasia of the
oesophageal mucosa.
• Predisposition to
Adenocarcinoma.
Prolonged reflux of gastric contents
Inflammation and ulceration of the squamous
epithelial lining
Healing of the lining by formation of intestinal
or gastric type epithelium – metaplasia.
This epithelium is better able to withstand the
effects of the gastric juices
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Can progress to dysplasia and adenocarcinoma
Its is an acquired condition due to gastro-oesophageal reflux
Bile reflux appears to be an important aetiological factor
10% of patients with GORD develop Barrett's oesophagus
Approximately 1% of patients with Barrett's oesophagus per
year progress to carcinoma
• Barrett's oesophagus increase the risk of cancer by x30
Clinical features
• Barrett's per se is usually asymptomatic
• Usually recognized as an incidental finding at
endoscopy
Barrett Esophagus Morphology
 Endoscopically, it appears as
“tongues” of red, velvety
mucosa above the GE junction
 Histologically, intestinal
metaplasia is composed of
goblet cells wit cytoplasmic
mucus vacuoles
 The diagnosis of Barrett
esophagus requires both:
Abnormal endoscopic findings
and histology of intestinal
metaplasia
Normal gastroesophageal junction
Barrett esophagus
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Conservative treatment
Lifestyle modification
Stop smoking
Avoid alcohol
Loose weight
Raise head of bed
Drug treatment
H2 antagonists
– Provide symptomatic relief in 60% at 6 weeks
– Endoscopic evidence of healing seen in only 40%
• Proton pump inhibitors
– 80% healing at 8 weeks
– More than 20% relapse despite maintenance therapy
– Long term therapy often required
Surgical options
• Indications:
– Recurrent symptomatic relapse
– Bile reflux
– Poor response to pharmacological
management
• Fundoplication is operation of choice performed as open or laparoscopic
procedure
Vascular lesions - Varices
• Dilatation of oesophageal
submucosal veins due to
portal hypertension
• Lower 3rd of the
oesophguse
• Presents with haematemsis
Strictures of the oesophagus
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Congenital
Reflux disease induced strictures
Corrosive poisoning
Tumors
• Rare – Scleroderma
Oesophageal Tumors
Benign
Leiomyoma
Malignant
Squamous Carcinoma 85%
Adenocarcinoma 15%
Oesophageal Carcinoma
• Adults > 50 years
• M:F = 4:1
• Geographical distribution - North China,
Iran, USSR, S. Africa
Squamous Carcinoma Predisposing
factors
– 1. Dietary - fungal contamination, High content of
nitrites / nitrosamines, def of Vit & trace metals
– 2. Oesophageal disorders - Achalasia cardia,
Diverticula, Oesophageal stasis.
– 3. Life style - Alcohol, Tobacco
– 4, Genetic - Epidermolysis Bullosa, Coeliac disease,
Ectodermal dysplasia
Clinical features
• PROGRESSIVE DYSPHAGIA UNTIL PROVED
OTHERWISE IS CARCINOMA OESOPHAGUS
• Regurgitation.
• Pain
• Loss of weight - BUT NOT LOSS OF APPETITE.
Morphology
• Site - Commonest in the middle 3rd.
• Macroscopy
– 1. Polypoidal fungating. ) 15%
– 2. Nodular mass.
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– 3. Diffuse infiltrative - flat lesion.
– 4. Excavated /ulcerated
– Superficial (in -situ)
Macroscopic Appearances
Microscopy
• Squamous carcinoma.
– Cell keratinization
– Intercellular bridges
/prickles.
– Keratin pearls.
Metastases
• Blood stream spread is uncommon. - Lung
Brain & Bone
• Lymph node – Upper 3rd - Cervical
– Middle 3rd - Mediastinal, tracheobronchial,
paratracheal
– Lower 3rd - Gastric & Coeliac node.
Causes of Death
• Starvation & wasting.
• Tracheo-oesophageal fistula - Aspiration
pneumonia.
• Rupture - Mediastinitis.
• Haemorrhage
• Distant spread.
Oesophageal carcinoma
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90% are squamous cell carcinomas
Occur in the upper or middle third of the oesophagus
8% are adenocarcinomas
Occur in the lower third of the oesophagus
Overall 5 year survival is very poor and is at best 20%
Less than 50% patients are suitable for potentially
curative treatment
• Of those undergoing 'curative' treatment less than
40% survive one year
Resectability and fitness for surgery assessed by:
• Chest x-ray
• Lung function tests(FEV1 > 1L)
• CT thorax & abdomen
• Liver ultrasound
• Endoscopic ultrasound
• Bronchoscopy
• Laparoscopy
Management
• Adenocarcinomas
• surgery is mainstay of treatment
• Upfront chemo irradiation may improve
survival
• Squamous cell carcinomas are more
responsive to radiotherapy
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Surgery
• Only 40% tumours are resectable
• Operative mortality now less than 10%
• Treatment should be in centres who perform
operation regularly
• Preoperative chemotherapy may be beneficial
Operative approaches
• Need 10 cm proximal clearance to avoid submucosal
spread.
• Total oesophagectomy via thoracoabdominal
approach (Adenocarcinoma)
• Subtotal two-stage oesophagectomy (Ivor-Lewis)
• Subtotal three-stage oesophagectomy (McKeown)
• Transhiatal oesophagectomy
Palliative treatment
• Aim to relieve obstruction and dysphagia with
minimal morbidity
Oesophageal intubation
– Endoscopic or radiological placement of stents are
now most commonly practiced
– Recent increased use of self-expanding stents
– Complications of stents
• Oesophageal perforation
• displacement or migration
• blockage due to ingrowth or overgrowth
• Laser therapy
– Produces good palliation in over 60% of cases
– May need to be repeated every 4 to 6 weeks
– Associated with oesophageal perforation in about 5%
cases
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External beam radiotherapy
Brachytherapy
Diathermy
Alcohol injection
Presentations of oesophageal disorders Symptoms
– Dysphagia – Difficulty in swallowing
• Organic disease (stricture and carcinoma)
• Motilitiy disorders –Dysphagia for liquids more likely
– Regurgitation
– Odynophagia – localized pain associated with swallowing
– Pain
• Heart burn – due to reflux
• Angina like tightening chest pain – occur in association with meals
– Waterbrash – mouth being full of fluid which is salty in taste
Presentations of oesophageal disorders –
Atypical symptoms
• Anaemia
• Pulmonary symptoms – due to aspiration
pneumonia in reflux
– Coughing
– Choking
– Repeated chest infections
Presentations of oesophageal disorders –
Physical signs
• Weight loss
• Pallor
• Neck swellings – pharyngeal pouch, enlarged
lymph nodes
• Chest signs on auscultation
• Epigastric mass – carcinoma of cardia
enlarging down
• Others – Tylosis, koilonychia
Evaluation of a patient with
dysphagia
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History
Physical examination
Investigations
History
Onset
Progression
Associated symptoms
Past history/associated disases
Examination
• For the cause – mouth, neck, larynx, neuro
• Effects – dehydration, malnutrition
investigations
• Imaging
• Endoscopy and biopsy
• Other
endoscopy
videofluorographic swallowing study
(VFSS)*
Management
Depend upon the cause
Definitive vs palliative
Endoscopic/surgical
Food & Drugs
Surgeries of Oesophagus
( Fundoplication)