Oesophagus

1
Oesophagus
2
Anatomical physiological considerations

• A muscular tube connecting pharynx to stomach.
• Guarded at both ends by sphincters.
• Lies anterior to cervical vertebrae in neck in
  posterior mediastinum in chest enters abdomen
  through oesophageal hiatus in diaphragm.
• The last 2-3 cm are within abdomen above GEJ with
  stomach.
• The mucosal lining of oesophagus is pale grey
  consists of squamous epithelium.
• The musculature of upper two-thirds of oesophagus
  is striated distal third is smooth.
• The oesophagus is devoid of a serosal layer.

3
Anatomical and physiological considerations

• The two sphincters are at the pharyngo-oesophageal
  junction (upper) in the region of the
  oesophageal opening (hiatus) in the diaphragm.
• Both have intrinsic extrinsic components.
• Upper intrinsic sphincter
• The main function of preventing access of air to
  the oesophagus working in conjunction with
  laryngeal closure during swallowing.
• It relaxes on initiation of the swallowing reflex
• The superior constrictor extrinsic component
  contracts to expel food or liquid into oesophagus
  where a wave of peristalsis carries it downwards.

4
Anatomical and physiological considerations

• Lower intrinsic sphincter is the circular smooth
  muscle of the oesophagus.
• Its role is to prevent GE regurgitation it is
  normally closed but relaxes in response to the
  swallowing wave.
• The intrinsic sphincter is supplemented by the
  striated muscle of the right crus, which splits
  to embrace the lower end of the oesophagus
  (keeping GEJ closed when intra-abdominal pressure
  is significantly increased).
• Another factor which prevents reflux from the
  stomach is the acute angle of insertion of the
  oesophagus into the stomach which brings the
  gastric and oesophageal walls in contact when
  intra-abdominal pressure rises.
• Anatomical disorders at the diaphragmatic hiatus
  reduce the efficacy of the intrinsic sphincter.

5
Anatomical relationships of the oesophagus
6
Clinical features of oesophageal diseaseSymptoms

• Dysphagia
• Difficulty in swallowing.
• Progressive
• A malignant growth or a stricture reduces size of
  oesophageal lumen
• Eventually goes on to total dysphagia when
  neither food, liquid nor the patient's own saliva
  can be swallowed.
• High grades of dysphagia are often associated
  with regurgitation into pharynx upper air
  passages therefore with respiratory infection.
• Non-progressive
• Disorders of function either of the whole
  oesophagus or at the lower sphincter.

7
Clinical features of oesophageal diseaseSymptoms

• Pain
• Pain is ill-localised in chest (retrosternal).
• May accompany partial dysphagia from obstruction.
• It also occurs in motility disorders.
• Confusion with pain originating in heart muscle
  is common.  
• Heartburn
• Heartburn is a retrosternal sensation of
  discomfort burning.
• Due to regurgitation from stomach into normally
  empty oesophagus.
• If there is considerable reflux, patient may
  feels presence of liquid in pharynx.

8
Clinical features of oesophageal diseaseSigns

• The deep situation of the oesophagus usually
  makes specific clinical features entirely absent.
• May accompany individual disorders.

9
Investigation

• Radiology
• Anteroposterior plain X-ray may occasionally show
  a broadening of the mediastinal shadow by a
  dilated oesophagus.
• An air-fluid level may be seen behind the heart
  if there is distal oesophageal obstruction.
• Contrast radiology, usually with barium sulphate
  but in special circumstances with a water-soluble
  contrast medium, is the standard method of
  establishing both anatomical functional
  abnormality.  
• Endoscopy
• The flexible oesophago-gastroduodenoscope is now
  often used as an alternative or complement to
  contrast radiology to achieve a diagnosis has
  the advantage of being able to take tissue for
  histological examination.

10
Investigation

• Manometry oesophageal pH studies
• Has an increasing role in the analysis of
  disorders of motility.
• Similar equipment can be used for monitoring acid
  level in oesophagus in patients with suspected
  reflux.
• The technique is to place a pH sensor at end of a
  tube in lower oesophagus to make continuous
  recordings over 24 hours.
• In normals there should be little change
  however, in those with reflux of acid contents,
  the pH falls sporadically, particularly at night.

11
Motility disorders

• Hypermotility chiefly diffuse spasm
• Hypomotility usually secondary to systemic
  sclerosis (scleroderma)
• Sphincter dysfunction the inability of lower
  sphincter to relax (achalasia).

12
HypermotilityDiffuse oesophageal spasm 

• Aetiology
• The cause is unknown (rare)
• Clinical features
• Intermittent, severe chest pain with dysphagia.
• DD angina pectoris.
• Investigation
• A contrast study shows exaggerated oesophageal
  contractions (corkscrew).
• Oesophagoscopy is usually normal, but manometry
  shows exaggerated contractions.  
• Management
• Drugs that reduce smooth muscle contraction
  (nitrates calcium channel blockers such as
  nifedipine) occasionally help.
• Balloon dilatation is also an option.
• Long oesophageal myotomy in which all layers of
  muscle down to mucosa are divided may be required.

13
Diffuse esophageal spasm
14
Diffuse esophageal spasm
15
HypermotilityNutcracker (super-squeeze)
oesophagus

• It is a common manometric finding in patients who
  present with chest pain which is of non-cardiac
  origin.
• The symptoms are the same as those for diffuse
  spasm, as is the management.
• However, surgical treatment is rarely required.

16
Hypomotility

• Systemic sclerosis
• Of unknown cause.
• The muscle layer is replaced by fibrous tissue.
• The presence of the disease may be suspected from
  other features such as loss of mobility of the
  face microvascular features, e.g. digital
  ischaemia.
• Investigation and management
• Contrast radiology shows diminished peristalsis
  confirmed by manometry.
• The treatment of hypomotility is that of the
  complications such as GER.

17
Achalasia (cardiospasm)

• Aetiology
• In the great majority of patients the cause is
  unknown, but a similar clinical condition is
  found in South America as a result of infection
  with a protozoan organism Trypanosoma cruzi.
• The lower sphincter fails to relax in response to
  the peristaltic wave, the bolus is partially
  retained in the oesophagus.

18
Achalasia

• Clinicopathological features
• Dilatation and muscular hypertrophy occur above
  the lower sphincter.
• Histological examination shows loss of ganglion
  cells.
• In long-standing cases the oesophagus becomes
  elongated inflamed mucosa from stasis of food ?
  ? development of malignant change.
•  
• Initially no frank dysphagia but rather a slowing
  down of normal rate of ingestion of food.
• Obvious dysphagia ultimately develops with
  retrosternal discomfort, regurgitation weight
  loss.
• Symptoms in later life may lead to confusion
  between achalasia carcinoma.

19
Achalasia

• Investigation
• Endoscopy is essential and in older patients may
  show a secondary cause such as infiltration of
  the distal oesophagus by malignant disease.
• Contrast study confirms delay at the lower
  sphincter, although in early symptomatic patients
  the abnormality may be difficult to identify.
• Manometry shows incomplete relaxation of lower
  sphincter in response to a swallow.

20
Primary achalasia
21
Primary achalasia
22
Secondary achalasia
23
Achalasia

• Management
• Balloon dilatation, which leads to resolution of
  symptoms in 80 although it may have to be
  repeated and carries a small risk of oesophageal
  perforation
• Longitudinal myotomy of the gastro-oesophageal
  junction (Heller's operation) which can be done
  either at open operation or via a laparoscope or
  thoracoscope anti-reflux procedure.
•  
• Surgical myotomy is associated with a small risk
  of GER but is otherwise a very satisfactory
  procedure.
• Endoscopic injection of botulinum toxin into
  oesophageal wall to paralyse LES.

24
Gastroesophageal reflux disorders

• Features of reflux occur in association with many
  different oesophageal conditions, including most
  of the motility disturbances.
• Reflux is particularly a symptom of abnormalities
  at the diaphragmatic hiatus.

25
Gastroesophageal reflux disorders

• Pathophysiological features
• If either acid or strongly alkaline secretions
  reach the lower oesophagus ? mucosal
  inflammation.
• Mostly a superficial oesophagitis.
• Stricture this is usually predominantly an
  inflammatory reaction in the mucosa submucosa,
  but it can, if inflammation takes place, become a
  fibrous narrowing
• Metaplastic change this leads to development of
  gastric-type columnar epithelium in lower
  oesophagus ('Barrett's oesophagus).
• It is a premalignant lesion (adenocarcinoma).

26
Gastroesophageal reflux disorders

• Clinical syndromes 
• Two main causes
• Hiatus hernia with reflux.
• Reflux without abnormal anatomy.

27
Hiatus hernia

• Types of hiatus hernia
• Sliding (usually associated with reflux)
  paraesophageal.
• Mixed (type III).

28
(a) The esophagogastric anatomy in a sliding
hiatus hernia.(b) The anatomy in a
paraesophageal hernia.
29
Sliding hiatus hernia

• The proximal stomach ascends into the chest
  through a lax or enlarged diaphragmatic opening,
  taking a circumferential cuff of peritoneum with
  it.
• The normally acute oesophagogastric angle is
  reduced, so that reflux is common even though the
  intrinsic lower sphincter is normal.
• Aetiology
• Obesity, increase in abdominal contents
  (pregnancy) ageing may be contributory factors.
• Clinical features
• There is postural reflux, heartburn
  occasionally some lower left chest pain.
• Vague indigestion is rarely caused by a sliding
  hernia.

30
Sliding hiatus herniaInvestigation

• Patients with the recent onset of symptoms,
  particularly if they are elderly, should be
  investigated for possible oesophagogastric
  cancer.
•  
• Contrast radiography
• The standard method of making the diagnosis is by
  barium swallow meal.
•  
• Endoscopy
• Although it is not always easy to identify the
  esophagogastric junction, this examination allows
  assessment of severity of oesophagitis, a
  tissue diagnosis by examination of a biopsy may
  be made in patients with Barrett's oesophagus.
•  
• pH Monitoring
• Oesophageal pH studies are useful in cases of
  diagnostic uncertainty and as a baseline
  measurement before surgical treatment.

31
Sliding hiatus herniaManagement

• Medical measures for the control of reflux
• Weight loss in the obese
• Sleeping with the head of the bed raised to avoid
  nocturnal reflux
• Alginate-containing antacids which are thought to
  reduce free liquid in the stomach and thus reduce
  the volume of reflux
• Acid reduction by H2-receptor antagonists (e.g.
  cimetidine or ranitidine) or proton pump
  inhibitors (e.g. omeprazole or lansoprazole).
• If these measures fail to control symptoms or the
  patient is not keen on long-term medication, then
  operation should be considered.

32
Sliding hiatus herniaManagement

• Surgical repair
• May be carried out at open operation or at
  laparoscopy.
• Reduction of the herniated stomach below the
  diaphragm
• Removal of the circumferential peritoneal sac
• Re-establishment of the esophagogastric angle
  reduction of the intercrural space by suturing
  the crura together behind the oesophagus an
  anti-reflux procedure-often loosely called a
  fundoplication.
• The last procedure is increasingly used although
  it may not always be justified. The fundus of the
  stomach is wrapped around the terminal oesophagus
  so that, as intra-abdominal pressure rises, the
  oesophagus is compressed (Fig. 18.3).
• Complication may be the inability to belch and
  bloating-a sensation of unrelieved fullness of
  the stomach.
• Some patients experience postoperative dysphagia,
  which is usually transient.

33
A fundoplication operationThe gastric fundus is
wrapped around the abdominal esophagus
34
Hiatus herniaPara-oesophageal hernia

• Aetiology
• A discrete peritoneal sac occurs at the left
  lateral border of oesophagus fundus of stomach
  rolls into this, sometimes carrying the EGJ into
  the chest.
• May cause a twist of the whole stomach-a gastric
  volvulus.
•  
• Clinical features
• Usually asymptomatic, although vague upper
  abdominal pain may occur.
• Incarceration going on to strangulation is not
  common but causes acute upper abdominal pain ?
  total dysphagia.
• This occurrence - usually in elderly frail
  individuals - is a surgical emergency.
•  
• Management
• Unless the patient is unfit, paraesophageal
  hernias should be repaired surgically because of
  the risk of strangulation.

35
Reflux without abnormal anatomy

• Aetiology and clinical features
• Symptoms of reflux without any demonstrable
  anatomical abnormality.
• In some, obesity is a factor others may have
  hyperchlorhydria with or without a demonstrable
  peptic ulcer.
• In the majority a definite cause is not
  identified.
• Features of heartburn dyspepsia, with
  regurgitation of gastric contents in some.
• Investigation
• Treated symptomatically without investigation.
• Those with troublesome features should have a
  barium swallow and endoscopy.
• Ambulatory monitoring of lower oesophageal pH may
  establish that there is persistent reflux, and
  oesophageal manometry identifies those with a
  motility disorder.
• Management
• Medical management.
• Oesophagitis which is unresponsive to treatment,
  an anti-reflux operation should be considered but
  only after careful assessment of the benefit that
  is likely to be achieved.

36
Oesophageal diverticula

• Hypopharyngeal pouch is the most common of these.
• Other diverticula in lower parts of the
  oesophagus are rare.

37
Oesophageal rupture mucosal tear (Mallory-Weiss
syndrome) Aetiology

• Aetiology
• Vomiting is usually a coordinated event. The
  stomach and diaphragm contract so that
  intragastric pressure is raised the oesophageal
  sphincters then relax, as does the oesophagus as
  a whole, and the stomach content is ejected.
• However, this orderly course may not take place
  if
• Voluntary inhibition is necessary
• Vomiting is artificially induced
• The individual is confused usually from
  excessive consumption of alcohol.
• In such circumstances, intragastric pressure
  forces stomach contents into the distal
  oesophagus, dilating it.
• The oesophagus may rupture with emptying of
  stomach contents into the left pleural cavity or,
  because the relatively elastic muscle has a
  greater capacity for stretch than does the folded
  mucosa and submucosa, only these are split to
  produce a longitudinal tear at the
  oesophagogastric junction.

38
Incomplete lower oesophageal tear (Mallory-Weiss
syndrome)

• The mechanism is the same as that for a complete
  tear.
• The history is typically of an initial blood-free
  vomit followed by bright red haematemesis later.
• Most episodes of bleeding from this cause are
  usually minor and self-limiting but are
  occasionally severe and persistent.
• If this is the case, the stomach is exposed,
  opened and the tear oversewn, nearly always with
  good results.

39
Oesophageal ruptureClinical features

• Clinical features  
• History
• Forceful vomiting may be with much intake of
  alcohol.
• Vomiting may also have been induced either in a
  glutton or in someone who is mentally disturbed
  with a history of excessive eating but with the
  paradoxical desire not to gain weight (bulimia).
• There will be sharp left-sided pleuritic pain.
•  
• Physical findings
• The effect of gastric content within the chest is
  to rapidly produce signs of severe sepsis with
  fever and circulatory disturbance.
• A left pleural effusion is present.
• The course is downhill with all the features of
  systemic inflammatory response syndrome.
• Occasionally, however, the rupture is localised
  and the patient is less ill with localised
  pleural signs and features of sepsis which are
  less severe.

40
Oesophageal ruptureClinical features

• Management
• In early rupture, the oesophagus is exposed and
  repaired.
• Gastrostomy is often done to drain gastric
  secretions.
• Parenteral or enteral (jejunostomy) nutrition is
  used until healing is assured.

41
Oesophageal ruptureMucosal tear

• Mucosal tear
• The presentation of this condition is with
  haematemesis.

42
Cancer of the esophagusEpidemiology

• Epidemiology
• This condition is relatively rare in the western
  world.
• In the Far East the incidence is in general much
  higher (China).
• Overall, the incidence is rising worldwide.

43
Cancer of the esophagusAetiology

• Squamous carcinoma
• The wide geographical variation in incidence has
  been attributed to social environmental
  factors.
• A strong association between cigarette alcohol
  consumption incidence of disease.
• Diet is of greatest importance.
• Three factors are recognised
• High intake of nitrosamines derived from nitrates
  used in food preservatives
• Low intake of both vitamin A nicotinic acid
• Iron deficiency anaemia, a known associate of
  hypopharyngeal cancer.
• Long-standing achalasia may lead to cancer ? due
  to stasis mucosal irritation.

44
Cancer of the esophagusAetiology

• Adenocarcinoma
• Cases of adenocarcinoma of the oesophagus now
  exceed those of squamous carcinoma in a ratio of
  21.
• Metaplastic change in the oesophageal mucosa from
  squamous to columnar epithelium as a result of
  reflux (Barrett's oesophagus) predisposes to
  development of adenocarcinoma.

45
Cancer of the esophagusPathological features

• Pathological features
• Nearly all lesions are a combination of narrowing
  ulceration.
• Spread by
• direct invasion first through full thickness of
  oesophageal wall and then into adjacent
  structures such as the trachea or bronchi, the
  pericardium, chest wall and diaphragm.
• submucosal infiltration both proximally
  distally
• lymph node involvement in the mediastinum and, in
  distal lesions, around the stomach. Upward spread
  in the mediastinum may produce a sentinel node in
  the supraclavicular fossa
• the bloodstream - distant metastases (liver, lung
  and brain).

46
Cancer of the esophagusClinical features

• Clinical features 
• Symptoms
• The mean duration of symptoms is 4-6 months but
  may be up to 3 years.
• Early ill-defined symptoms
• There may be a feeling of something stuck in the
  oesophagus.
• Retrosternal discomfort, belching dyspepsia.

47
Cancer of the esophagusClinical features

• Progressive dysphagia
• The most common presenting symptom (2/3 of
  oesophageal diameter).
• In the early stages, dysphagia is for solids
  only, later difficulty with liquids.
• Regurgitation after eating
• May be delay until dysphagia is total (inability
  to swallow saliva).
• Weight loss
• More than 10-15 of the pre-illness weight may be
  lost over 4-6 weeks.
•  
• Acute obstruction
• Precipitated by the impaction of a large
  (inadequately chewed) food bolus.

48
Cancer of the esophagusClinical features

• Miscellaneous
• A long history of heartburn suggestive of acid
  reflux in patients with an adenocarcinoma in an
  area of columnar metaplasia.
• Pain may indicate penetration of tumour outside
  wall of oesophagus.
• Productive cough, particularly at night, due to
  aspiration of retained material into respiratory
  tract or by development of a malignant
  oesophagotracheal fistula.
• Hoarseness may mean involvement of the recurrent
  laryngeal nerve.
• Features of distant metastases can be the cause
  of presentation.

49
Cancer of the esophagusClinical features 

• Signs
• Clinical examination of a patient with localised
  oesophageal cancer usually does not reveal any
  abnormalities other than evidence of recent
  weight loss.
• Total dysphagia is associated with signs of lack
  of water - reduced skin turgor a coated furred
  tongue.
• Signs of dissemination
• Palpable lymphadenopathy, usually in
  supraclavicular region.
• Hepatomegaly, jaundice, ascites, cardiac
  arrhythmias features of pulmonary
  consolidation.
• Respiratory infection due to aspiration of
  oesophageal content.

50
Cancer of the esophagusInvestigation

• Investigation
• Radiography
• Barium swallow
• simplicity
• relative lack of expense
• high sensitivity in diagnosis of a stricture
• accurate determination of the anatomical site
• definition of the anatomy of the stomach
  duodenum
• creation of a 'road map' for endoscopy.

51
Cancer of the esophagusInvestigation

• Endoscopy
• With a flexible instrument under local
  anaesthesia or sedation.
• Allows
• biopsy and brush cytology
• assessment (partial) of the extent of the lesion
• concurrent dilatation temporary relief of
  obstruction
•  
• Dangers
• perforation of a growth - unlikely unless
  dilatation is undertaken

52
Cancer of the esophagusInvestigation

• Once the diagnosis is confirmed, further study to
  assess stage of disease to determine the
  suitability of the patient for operative
  treatment.
•  
• Ultrasound examination
• May demonstrate liver metastases enlarged LN.
• Endoscopic ultrasound, can measure depth of
  penetration of growth into oesophageal wall
  assess enlargement of mediastinal LN.
•  
• Computerised tomography
• CT scan of chest abdomen may
• detect metastases
• determining size of the primary
• attachment to surrounding structures
• A fistula into air passages may be detected
  (bronchoscopy for confirmation).

53
Cancer of the esophagusScreening

• Screening
• In places where the incidence is high (such as
  China Japan), routine flexible oesophagoscopy
  and/or obtaining oesophageal specimens for
  cytology are increasingly being recommended to
  detect early asymptomatic disease.

54
Cancer of the esophagusManagement - Surgical
resection

• Surgical resection
• Surgical resection of oesophageal cancer is
  confined to patients with 'operable'
  disease-locally removable cancer and no
  detectable metastatic disease who are
  considered fit enough for the major operation
  required.
• There is good evidence now that neoadjuvant
  chemotherapy, sometimes combined with
  radiotherapy, increases the frequency of complete
  cancer excision significantly improves overall
  survival rates and disease free interval.
• Such multimodal treatment is now standard
  practice.

55
Cancer of the esophagus Management - Surgical
resection

• Contraindications to surgery include
• poor cardiovascular, pulmonary or renal function
• tracheo-oesophageal fistula
• other evidence of advanced local disease
• irremovable or multiple metastatic disease.
• Asymptomatic and small metastases may, on
  occasion, not be a contraindication to the
  restoration of satisfactory swallowing by
  resection, but other methods should be
  considered.
• The principles of resection with cure in mind
  are
• wide resection margins
• radical lymph node clearance within the chest and
  for distal growths at the oesophagogastric
  junction also in the upper abdomen.

56
Cancer of the esophagus Management - Surgical
resection

• Open operation which may involve opening both the
  abdomen and thorax.
• Trans-hiatal removal.
• The abdomen alone is opened and the oesophagus
  freed in the chest by blunt dissection through
  the diaphragmatic hiatus.
• Stomach or colon for reconstruction is then
  passed through the posterior mediastinum to the
  neck where it is anastomosed to the upper
  oesophagus through a cervical incision.
• This procedure is used by some surgeons for
  patients with Barrett's esophagus containing
  high-grade dysplasia and thus having a very high
  risk of developing adenocarcinoma.
•  
• Endoscopic removal.
• By dissection within the chest (thorascopy) and
  abdomen (laparoscopy).

57
Cancer of the esophagusManagement

• Other methods of restoring swallowing 
• Radiotherapy for squamous carcinoma. Relief is
  not immediate, is usually temporary and up to
  one-third of patients develop a fibrous
  stricture.
• Chemotherapy (e.g. with 5-fluorouracil 5-FU and
  cisplatin), either alone or preferably in
  combination with radiotherapy, may lead to total
  disappearance of the local tumour in 30 of
  patients.
• Combined radiochemotherapy is increasingly used
  as neoadjuvant therapy prior to surgical
  resection, and is used in some centres as primary
  radical treatment for squamous carcinoma.
  Resection in these cases is reserved for local
  recurrent or residual cancer after
  radiochemotherapy.
•  
• Dilatation intubation with a large, specially
  designed tube were formerly popular. However,
  fracture of the growth with later perforation was
  not uncommon and often fatal the quality of
  swallowing was not very good regurgitation and
  aspiration could occur and, in distal tumours,
  migration of the tube into the stomach frequently
  took place. Such tubes have now been replaced by
  self-expanding metal endoprosthesis some of
  which are covered with a plastic membrane and
  carry fewer problems of insertion and the
  possibility of better palliation.
• Local endoscopic destruction of the tumour by
  laser or argon-beam diathermy, which can be
  repeated.

58
Cancer of the esophagusPrognosis

• Prognosis
• The outcome of resection depends on the stage of
  the growth.
• When tumour is confined to the mucosa, a 5-year
  survival of 60 is possible, but any further
  spread means a fall-off to less than 5 for
  growths that have penetrated the full thickness
  of the gullet.
• Combined regimens of resection and neoadjuvant
  combinations of radiotherapy and chemotherapy are
  producing improved results.