Oesophagus Flashcards
Embryology of oesophagus
- sources
- time frame
- change in length
- arterial supply
From two sources: pharyngeal gut and pregastric foregut
4 weeks: respiratory diverticulum
Closure of diverticulum by tracheo-oseophageal folds, caudally to cranially
Forms the tracheo-oesophageal septum
As the embryo grows the oesophagus lengthens and lumen is vacuolised
Blood supply cranially from branchial arteries, caudally from aortic branches
Constrictions of oesophagus
15-17cm - upper oesophageal sphincter (pharyngeo-oesophageal constriction)
23cm - aortobronchial constriction
38-40cm - lower oesophageal sphincter (diaphragmatic constriction)
AJCC divisions of oesophagus and measurements
Cervical: 0-18cm, hypopharynx to thoracic inlet (incl UOS)
Upper thoracic: 19-24cm, thoracic inlet to inferior border of azygos vein
Middle thoracic: 24-32cm, inferior border of azygous vein to inferior pulmonary veins
Lower thoracic: 32-40cm, inferior pulmonary veins to stomach (incl LOS)
Antireflux structures of the GOJ (7)
- Lower oesophageal sphincter
- Angle of His: sling of oblique fibres in gastric cardiac musculature along with clasp of circular fibres in the distal oesophagus: contract to make the angle more acute
- Pinchcock action of diaphragmatic crura
- Rosette of loose oesophageal mucosa around the GOJ
- Length of intra-abdominal oesophagus
- Gastro-oesophageal flap valve: angle of entry of oesophagus into stomach
Layers of the oesophagus (7)
Mucosa: non-keratinised stratified squamous epithelium + inflammatory cells
- at GOJ is columnar epithelium
Lamina propria: contains blood vessels, lymphatics and nerves + inflammatory cells
Muscularis mucosa: allows crinkling of the mucosa in a non-distended state
Submucosa: loose connective tissue, mucus-secreting glands, Meissner plexus (specialised nerve cells)
Muscularis propria: deep circular and superficial longitudinal
Loose adventitia but no serosa
Where do motility disorders of the oesophagus affect and why?
Distal oesophagus - they are disorders of smooth muscle
Arterial supply of the oesophagus (5)
Segmental
- inferior thyroid, carotid, subclavian, thyrocervical, costocervical, superior thyroid,vertebral
- bronchial arteries (branches of the aorta)
- broncho-oesophageal artery (inconstant)
- inferior phrenic
- left gastric
Form rich anastomoses within the submucosa
Lymphatic drainage of the oesophagus: pattern, and orders of nodes (3)
45% drain directly into thoracic duct
Above and below the tracheal bifurcation the lymphatics split
- up to paratracheal and cervical nodes
- down to lower mediastinal and coeliac nodes
I: para-oesophageal nodes - within para-oesophageal fatty tissue
II: mediastinal nodes - aorta, deep cervical and supraclavicular, lesser curvature, left gastric, coeliac plexus
III: peripheral nodes - lateral clavicular, pulmonary hilar, splenic hilar, greater curvature, common hepatic artery
Phrenico-oesophageal ligament
- components (4)
- attachments
- function
- age-related changes
A condensation of pleura, endothoracic fascia, transversalis fascia, and peritoneum
Upper: inserts into muscular layer of lower 1-3cm of the oesophagus
Lower: inserts into cardia
- separated from GOJ by fat pad and connective tissue
Function: Airtight seal between thorax and abdomen; barrier between negative intrathoracic pressure and positive abdominal pressure
Weakening of inferior leaf with age: ligament ascends into thorax
Crura
- origin
- structure of left and right
- sling composition
- 1st 4 lumbar vertebrae
- left does not divide
- right: superficial will lazily move anteromedially to join central tendon; deep will form sling around oesophagus as it enters the abdomen (oesophageal hiatus, T10)
- composition: 60% all right crus, 40% some fibres of left crus
Nerve supply of the oesophagus
Parasympathetic: vagal trunks, cervical plexus, oesophageal plexi on anterior and posterior wall; small branches of CNIX and XI
Sympathetic: T4-6
Meissners plexus in submucosa
Auerbachs (myenteric) plexus between circular and longitudinal layers
Non-iatrogenic causes of oesophageal perforation (4)
Caustic (early or delayed, liquefactive necrosis, NG/OGD to assess)
Foreign body (early or delayed, sharp or food bolus)
Spontaneous/Boerhaave’s (vomiting, laughing, lifting, gagging)
Traumatic (usually penetrating, surrounding structures need fixing)
Iatrogenic causes of oesophageal perforation (7)
Who is at increased risk
OGD (therapeutic more likely, side viewing scopes)
EMR, ESR
Intubation
NG placement
Dilatation
Stent (delayed complications - fistulae)
Surgery (endarterectomy, thyroid, tracheostomy, thoracic and gastric surgery incl fundoplication and myotomy)
Increased risks: cervical rib, Zenkers, radiation, strictures, neoplasm
Surgical techniques for oesophageal perforation
Cervical oesophagus: oblique left neck incision, retract SCM laterally and divide omohyoid and middle thyroid vein, retract trachea medially, expose with blunt dissection
Mid-thoracic oesophagus: right thoracotomy in 4-7 intercostal space, retract lung anteriorly, penrose drain to encircle oesophagus
Distal thoracic oesophagus: left posterolateral thoracotomy in 6-8 intercostal space
Abdominal oesophagus: midline laparotomy, retract left liver to right, divide short gastrics, use fundus as buttress for repair
Presentation of oesophageal perforation according to location
Cervical oesophagus: left neck abscess, drooling, odynophagia
Upper and mid-thoracic oesophagus: right empyema, mediastinitis, pneumothorax
Distal thoracic oesophagus: left empyema, mediastinitis, pneumothorax; may have peritonism
Abdominal oesophagus: peritonism
Endoscopic techniques for treatment of oesophageal perforation
Stent (large, can migrate if no tumour, can’t use for cervical oes)
Through the scope clips (small, mucosa only)
Over the scope clips (large diameter, full-thickness closure, can cause perf when passing)
Vacuum-assisted (for small, non-septated defects, suction of secretions and granulation, change foam every 2-3 days)
Why place a chest drain following oesophageal repair? Where?
Posteriorly, next to vertebrae
To promote lung expansion, evacuate pneumothorax, prevent empyema, detect and drain any further leak
Use Blake or Jackson Pratt drain in abdomen for distal tear
Surgical treatments for achalasia; pros and cons
- Pneumatic dilatation:
- least invasive, lasts 4 years, cost effective
- needs redo, gets less and less effective, perforation - Heller myotomy
- combined with antireflux procedure, effective, long lasting
- surgical, risk of perf/ptx/vagal injury - POEM (peroral endoscopic myotomy)
- cut fibres of LOS to cardia submucosally; less invasive, good for type III (spasmodic) achalasia
- risk of perforation, no anti-reflux procedure
What is the pathophysiology of achalasia?
Achalasia is an oesophageal motility disorder characterised by dysphagia to solids and liquids, regurgitation and symptoms of GORD
Due to hypertension of the LOS and aperistaltic distal oesophagus
Thought to be neurodegenerative, arising from an auto-immune process attacking the myenteric ganglia within the muscular wall of the oesophagus
Sclerosant of choice for treatment of oesophageal varices
5% ethanolamine oleate
Treatment of oesophageal varices (steps) (10)
Resuscitation: IVL, fluids, blood/clotting factors
Intubation
NG tube
Erythromycin: prokinetic
Ceftriaxone: antibiotic
Terlipressin: vasopressin analogue, causes mesenteric constriction and decrease in portal blood flow
Balloon tamponade (a step toward definitive management)
Endoscopy: band ligation or sclerotherapy
TIPS
Portocaval/surgical shunt
Liver transplant
Los Angeles classification of reflux oesophagitis
LA grade A: one or more mucosal breaks, <5mm length
LA grade B: one or more mucosal breaks, >5mm but not continuous over mucosal folds
LA grade C: at least one break continuous over the mucosal fold but not more than 75% circumference
LA grade D: mucosal break involving >75% circumference
What is the pathophysiology by which Barretts oesophagus transforms from metaplasia to adenocarcinoma?
40% through traditional pathway of gradual sequence of genetic alterations associated with dysplastic changes of increasing severity
60% through chromosomal instability in Barretts metaplastic cells - allow cancer to develop rapidly (even between surveillance intervals) - genomic doubling
Adenocarcinoma incidence in patients with Barretts
0.1-3% of those with Barretts have adenocarcinoma
30-fold risk above general population
Barretts patients often die of non-cancer related causes (obesity, cardiac, age)
