Esophageal disorders

OESOPHAGUS

Surgical anatomy

The oesophagus is a muscular tube, approximately 25 cm long, mainly occupying the posterior mediastinum and extending from the upper oesophageal sphincter (the cricopharyngeus muscle) in the neck to the junction with the cardia of the stomach.
The musculature of the upper oesophagus, including the upper sphincter, is striated. This is followed by a transitional zone of both striated and smooth muscle with the proportion of the latter progressively increasing so that, in the lower half of the oesophagus, there is only smooth muscle.
It is lined throughout with squamous epithelium. The parasympathetic nerve supply is mediated by branches of the Vagus nerve that has synaptic connections to the myenteric (Auerbach’s) plexus.

FOREIGN BODIES IN THE OESOPHAGUS

All manner of foreign bodies have become arrested in the oesophagus. The most common impacted material is food, and this usually occurs above a significant pathological lesion so the cause of impaction must then be investigated. Plain radiographs are often useful for foreign bodies, but impacted materials are not always radiopaque. Foreign bodies that have become stuck in the oesophagus should be removed by flexible endoscopy . If the object may injure the oesophagus on withdrawal, an over tube can be used.
Button batteries can be a particular worry as they are difficult to grasp, and it is tempting to push them on into the stomach.

PERFORATION

Perforation of the oesophagus is usually iatrogenic (at therapeutic endoscopy) or due to ‘barotrauma’ (spontaneous perforation).
Many instrumental perforations can be managed conservatively, but spontaneous perforation is often a life-threatening condition that requires surgical intervention.

Instrumental perforation

Instrumentation is by far the most common cause of perforation. Modern instrumentation is remarkably safe, but perforation remains a risk that should never be forgotten .
Perforation related to diagnostic upper gastrointestinal endoscopy is unusual. A number of patient-related factors are associated with increased risk, including large anterior cervical osteophytes, the presence of a pharyngeal pouch and mechanical causes of obstruction. Patients undergoing therapeutic endoscopy have a perforation risk that is at least 10 times greater than those undergoing diagnostic endoscopy.


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 localised to the neck, hoarseness, painful neck movements and subcutaneous emphysema. Intrathoracic and intra-abdominal perforations, which are more common, can give rise to immediate symptoms and signs either during or at the end of the procedure, including chest pain, haemodynamic instability, patients may additionally complain of abdominal pain or respiratory difficulties.
There may be evidence of subcutaneous emphysema, pneumothorax or hydropneumothorax. In some patients, the diagnosis may be missed and recognised 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 recognised immediately, then early and late suspected perforations should be assessed by a water-soluble contrast swallow. A CT scan can be used to replace a contrast swallow or as an adjunct to accurately delineate specific fluid collections.

Barotrauma (spontaneous perforation, Boerhaave syndrome)

This occurs classically when a person vomits against a closed glottis. The pressure in the oesophagus increases rapidly, and the oesophagus bursts at its weakest point in the lower third, sending a stream of material into the mediastinum and often the pleural cavity as well.
Boerhaave syndrome is the most serious type of perforation because of the large volume of material that is released under pressure. This causes rapid chemical irritation in the mediastinum and pleura followed by infection if untreated.

Diagnosis of spontaneous perforation

The clinical history is usually of severe pain in the chest or upper abdomen following a meal or a bout of drinking. Associated shortness of breath is common. Many cases are misdiagnosed as myocardial infarction or perforated peptic ulcer. There may be a surprising amount of rigidity on examination of the upper abdomen, even in the absence of any peritoneal contamination.
A chest X-ray is often confirmatory with air in the mediastinum, pleura or peritoneum. A contrast swallow or CT is nearly always required to guide management .

Treatment of oesophageal perforations

Perforation of the oesophagus usually leads to mediastinitis. The loose areolar tissues of the posterior mediastinum allow a rapid spread of gastrointestinal contents. The aim of treatment is to limit mediastinal contamination and prevent or deal with infection.
The decision between operative and non-operative management rests on four factors:
1 the site of the perforation (cervical vs. thoracoabdominal);
2 the event causing the perforation (spontaneous vs. instrumental);
3 underlying pathology (benign or malignant);
4 the status of the oesophagus before the perforation (fasted and
empty vs. obstructed with a stagnant residue).
So most perforations that can be managed non-operatively are the small instrumental perforations of a clean oesophagus without obstruction, where leakage is likely to be confined to the nearby mediastinum at worst.
The principles of non-operative management involve hyperalimentation, preferably by an enteral route, nasogastric suction and broad-spectrum intravenous antibiotics.


For patients requiring surgery, the choice rests between direct repair, the creation of an external fistula or, rarely, oesophageal resection with delayed reconstruction.
On-going luminal obstruction (often related to malignancy) in a patient unfit for major surgery can be dealt with by placement of a self-expanding stent.

MALLORY–WEISS SYNDROME

Forceful vomiting may produce a vertical split in the gastric mucosa, immediately below the squamocolumnar junction at the cardia in 90% of cases. In only 10% is the tear in the oesophagus . The condition presents with haematemesis. Usually, the bleeding is not severe, but endoscopic injection therapy may be required for the occasional, severe case. Surgery is rarely required.

CORROSIVE INJURY

Corrosives such as sodium hydroxide (caustic soda) or sulphuric acid may be taken in attempted suicide. Accidental ingestion occurs in children and when corrosives are stored in bottles labelled as beverages.
The type of agent, its concentration and the volume ingested largely determine the extent of damage. In general, alkalis are relatively odourless and tasteless, making them more likely to be ingested in large volume.
Alkalis cause liquefaction and saponification of fats. Acids cause coagulative necrosis with eschar formation, and this coagulant may limit penetration to deeper layers of oesophageal wall. Acids also cause more gastric damage than alkalis because of the induction of intense pylorospasm with pooling in the antrum.
The key to management is early endoscopy by an experienced endoscopist to inspect the whole of the oesophagus and stomach . Deep ulcers and the recognition of a grey or black eschar signify the most severe lesions with the greatest risk of perforation. Minor injuries with only oedema of the mucosa resolve rapidly with no late sequelae. These patients can safely be fed. With more severe injuries, a feeding jejunostomy may be appropriate until the patient can swallow saliva satisfactorily.
The widespread use of broad-spectrum antibiotics and steroids is not supported by evidence.
Regular endoscopic examinations are the best way to assess stricture development . Significant stricture formation occurs in about 50% of patients with extensive mucosal damage .
There is a controversy regarding the risk of developing carcinoma in the damaged oesophagus and stomach. The lifetime risk is less than 5%.