Oesophagus , stomach and salivary glands

• Oesophagus


  Muscular tube, approximately 25 cm long, extending from the upper oesophageal sphincter in the neck to the junction with the cardia of the stomach, mainly occupying the posterior mediastinum
• Oesophageal musculature


  • Outer longitudinal and inner circular layer
  • Upper 2 to 6 cm contains only striated muscle fibers
  • Smooth muscle fibers gradually become more abundant from there on
• Oesophageal lining


  Lined throughout with squamous epithelium
• Oesophageal nerve supply


  • Parasympathetic nerve supply mediated by branches of the vagus nerve that has synaptic connections to the myenteric (Auerbach's) plexus
  • Meissner's submucosal plexus is sparse in the oesophagus
• Upper oesophageal sphincter


  • Consists of powerful striated muscle
  • Normally closed at rest
  • Serves as a protective mechanism against regurgitation of oesophageal contents into the respiratory passages
  • Stops air entering the oesophagus other than the small amount that enters during swallowing
• Lower oesophageal sphincter (LOS)

  • More subtle, created by the asymmetrical arrangement of muscle fibers in the distal oesophageal wall just above the oesophagogastric junction
  • A zone of relatively high pressure that prevents gastric contents from refluxing into the lower oesophagus
  • Opens in response to a primary peristaltic wave
  • Relaxes to allow air to escape from the stomach and at the time of vomiting
• Blood supply to the oesophagus

  • Cervical portion receives main blood supply from the inferior thyroid artery
  • Thoracic portion receives blood supply from the bronchial arteries, with 75% of individuals having one right-sided and two left-sided branches, and two esophageal branches arising directly from the aorta
  • Abdominal portion receives blood supply from the ascending branch of the left gastric artery and from inferior phrenic arteries
• Oesophageal blood vessels


  • On entering the wall of the esophagus, the arteries assume a T-shaped division to form a longitudinal plexus, giving rise to an intramural vascular network in the muscular and submucosal layers
• Drainage of oesophageal veins

  • In the cervical region, they empty into the inferior thyroid vein
  • In the thoracic region, they empty into the bronchial, azygos, or hemiazygos veins
  • In the abdominal region, they empty into the coronary vein
• Oesophageal lymphatics


  • Lymph flow in the submucosal plexus runs in a longitudinal direction
  • In the upper two-thirds of the oesophagus, the lymphatic flow is mostly cephalad, and, in the lower third, caudad
  • In the thoracic portion, the submucosal lymph plexus extends over a long distance in a longitudinal direction before penetrating the muscle layer to enter lymph vessels in the adventitia
  • The cervical oesophagus has a more direct segmental lymph drainage into the regional nodes
• Foreign bodies in the oesophagus

  • The most common is a food bolus, which usually signifies underlying disease
  • It is usually possible to remove foreign bodies by flexible endoscopy using suitable grasping forceps, a snare or a basket
  • If the object may injure the oesophagus on withdrawal, an overtube can be used, and the endoscope and object can be withdrawn into the overtube before removal
  • Beware of button batteries in the oesophagus as the exhausted battery may rapidly corrode in the gastrointestinal tract and is best extracted
  • Impacted food bolus will often break up and pass on if the patient is given fizzy drinks and confined to fluids for a short time
• Causes of oesophageal perforation

  • Traumatic (usually iatrogenic at therapeutic endoscopy, penetrating or blunt injury, foreign bodies)
  • Swallowing corrosives
  • Barotrauma (spontaneous perforation, Boerhaave syndrome)
  • Pathological (ulcers or tumours)
• Boerhaave syndrome


  Spontaneous perforation of the oesophagus, the most serious type of perforation because of the large volume of material that is released under pressure, causing rapid chemical irritation in the mediastinum and pleura followed by infection if untreated
• Diagnosis of spontaneous perforation

  • Severe pain in the chest or upper abdomen following a meal or a bout of drinking
  • Associated shortness of breath is common
  • May be misdiagnosed as myocardial infarction, perforated peptic ulcer or pancreatitis if the pain is confined to the upper abdomen
  • Surprising amount of rigidity on examination of the upper abdomen, even in the absence of any peritoneal contamination
  • Chest X-ray often confirmatory with air in the mediastinum, pleura or peritoneum
  • Pleural effusion occurs rapidly either as a result of free communication with the pleural space or as a reaction to adjacent inflammation in the mediastinum
  • Contrast swallow or CT is nearly always required to guide management
• Pathological perforation


  • Free perforation of ulcers or tumours of the oesophagus into the pleural space is rare
  • Erosion into an adjacent structure with fistula formation is more common, with aerodigestive fistula being the most common, usually encountered in primary malignant disease of the oesophagus or bronchus
• Penetrating injury perforation


  Perforation by knives and bullets is uncommon, even in war, as the oesophagus is a relatively small target surrounded by other vital organs
• Instrumental perforation


  • Instrumentation is by far the most common cause of perforation
  • Perforation related to diagnostic upper gastrointestinal endoscopy is unusual, but can occur usually at sites of pathology or when the endoscope is passed blindly
  • Risk factors include large anterior cervical osteophytes, the presence of a pharyngeal pouch and mechanical causes of obstruction, as well as biopsy of a malignant tumour and therapeutic endoscopy procedures
  • The oesophagus may be perforated by guidewires, graduated dilators or balloons, or during the placement of self-expanding stents
• Diagnosis of instrumental perforation

  • In most cases, a combination of technical difficulties and an interventional procedure should lead to a high index of suspicion
  • Cervical perforation may result in pain localized to the neck, hoarseness, painful neck movements and subcutaneous emphysema
  • Intrathoracic and intra-abdominal perforations can give rise to immediate symptoms and signs, including chest pain, haemodynamic instability, oxygen desaturation or visual evidence of perforation
  • Within the first 24 hours, patients may additionally complain of abdominal pain or respiratory difficulties, subcutaneous emphysema, pneumothorax or hydropneumothorax
  • The diagnosis may be missed and recognized only at a late stage beyond 24 hours, as unexplained pyrexia, systemic sepsis or the development of a clinical fistula
  • Careful endoscopic assessment at the end of any procedure combined with a chest X-ray will identify many cases of perforation immediately
  • If not recognized immediately, then early and late suspected perforations should be assessed by a water-soluble contrast swallow, and if this is negative, a dilute barium swallow should be considered
  • A CT scan can be used to replace a contrast swallow or as an adjunct to accurately delineate specific fluid collections
• Treatment of oesophageal perforations

  • The aim is to limit mediastinal contamination and prevent or deal with infection
  • Can be either operative or non-operative treatment
  • The decision between operative and non-operative management rests on the site of the perforation, the event causing the perforation, underlying pathology, and the status of the oesophagus before the perforation
• Non-operative management of oesophageal perforations

  • Most perforations that can be managed non-operatively occur in the context of small instrumental perforations of a clean oesophagus without obstruction, where leakage is likely to be confined to the nearby mediastinum at worst
  • Cameron's criteria for non-operative management: barium swallow shows perforation contained within the mediastinum and draining well back into the esophagus, symptoms are mild, and there is minimal evidence of clinical sepsis
  • Instrumental perforations in the cervical oesophagus are usually small and can nearly always be managed conservatively, with development of a local abscess being an indication for cervical drainage
  • Conservative management of an instrumental perforation in the thoracoabdominal parts of the oesophagus can be undertaken when the perforation is detected early and prior to oral alimentation
• Principles of non-interventional management

  • Hyperalimentation, preferably by an enteral route
  • Nasogastric suction
  • Broad-spectrum intravenous antibiotics
• Indications for surgical management

  • Patient is unstable with sepsis or shock
  • Evidence of a heavily contaminated mediastinum, pleural space or peritoneum
  • Widespread intrapleural or intraperitoneal extravasation of contrast material
  • Ongoing luminal obstruction (often related to malignancy) in a frail patient considered unfit for major surgery, which can be dealt with by placement of a covered self-expanding stent
• Surgical management options


  • Direct repair, if the perforation is recognized early (within the first 4–6 hours) and the extent of mediastinal and pleural contamination is small
  • Deliberate creation of an external fistula, for late presentation and in the presence of widespread mediastinal and pleural contamination
  • Oesophagectomy, in unusual circumstances with extensive necrosis following corrosive ingestion, with oesophagostomy and gastrostomy performed with a view to delayed reconstruction
• Mallory-Weiss syndrome


  • Vertical split in the gastric mucosa immediately below the squamocolumnar junction at the cardia, rather than a full perforation, caused by vigorous vomiting in a patient with a hiatal hernia
  • Characterized by arterial bleeding, which may be massive
  • Vomiting is not an obligatory factor, as there may be other causes of an acute increase in intra-abdominal pressure, such as paroxysmal coughing, seizures, and retching
  • Presents with haematemesis, usually not severe but may require endoscopic injection therapy of epinephrine in severe cases
  • Surgery is rarely required, consisting of laparotomy and high gastrotomy with oversewing of the linear tear
• Intramural rupture


  Dissection within the oesophageal wall that causes severe chest pain, often with odynophagia
• Esophagostomy


  Should be performed with a view to delayed reconstruction
• Mallory-Weiss syndrome


  Vertical split in the gastric mucosa rather than a full perforation immediately below the squamocolumnar junction at the cardia in 90% of cases. In only 10% is the tear in the oesophagus
• Mallory-Weiss tears


  • Characterized by arterial bleeding, which may be massive
  • Vomiting is not an obligatory factor, as there may be other causes of an acute increase in intra-abdominal pressure, such as paroxysmal coughing, seizures, and retching
• Mallory-Weiss syndrome presentation


  1. Haematemesis

  2. Usually the bleeding is not severe, but endoscopic injection therapy of epinephrine may be required for the occasional, severe case

  3. Surgery is rarely required
• Intramural haematoma


  Seen most often in elderly patients on anticoagulants or patients with coagulation disorders, and usually follows an episode of vomiting
• Management of intramural rupture and intramural haematoma

  1. Can be managed conservatively

  2. Symptoms usually resolve in 7–14 days, and oral intake can be reinstituted as soon as symptoms allow
• Caustic injury


  Swallowing of caustic substances causes an acute and a chronic injury
• Phases of lesions caused by lye injury

  1. Acute necrotic phase (1 to 4 days after injury)

  2. Ulceration and granulation phase (3 to 5 days after injury)

  3. Cicatrization and scarring phase (begins the third week following injury)
• Alkalies vs acids


  • Alkalies dissolve tissue and penetrate more deeply, while acids cause a coagulative necrosis that limits their penetration
• Clinical manifestations of caustic injury


  • In the initial phase: pain in the mouth and substernal region, hypersalivation, odynophagia, and dysphagia, fever, bleeding, vomiting
  • In the cicatrization and scarring phase: dysphagia due to fibrosis and retraction, resulting in narrowing of the esophagus
• Early management of caustic injury


  1. Administering neutralizing agents within the first hour

  2. Correcting hypovolemia and administering broad-spectrum antibiotics

  3. Inserting a feeding jejunostomy tube if necessary

  4. Starting oral feeding when the dysphagia of the initial phase has regressed
• Grading of caustic injury

  • First degree: Mucosal hyperemia and edema
  • Second degree: Limited hemorrhage, exudate ulceration, and pseudomembrane formation
  • Third degree: Sloughing of mucosa, deep ulcers, massive hemorrhage, complete obstruction of lumen by edema, charring, and perforation
• Long-term management of caustic injury


  1. Esophagoscopy and dilations initiated if strictures are present

  2. Antegrade dilation with a Hurst or Maloney bougie and retrograde dilation with a Tucker bougie

  3. Surgical intervention if an adequate lumen cannot be established or maintained
• Classification of oesophageal motility disorders

  • Disorders of the pharyngo-oesophageal junction
  • Disorders of the body of the oesophagus
  • Disorders of the lower oesophageal sphincter
• Achalasia


  Uncommon condition due to loss of the ganglion cells in the myenteric (Auerbach's) plexus, the cause of which is unknown