Oesophageal perforation can be caused by external trauma or any instrument, device, or foreign body reaching the hypopharynx.

Laceration and rupture of the lower oesophagus or the gastro-oesophageal junction are also associated with forceful or prolonged emesis. Since the original description of Boerhaave, the term ‘spontaneous’ rupture of the oesophagus has been used almost routinely in the literature to include all perforations involving the entire thickness of the oesophageal wall and associated with emesis. Mallory and Weiss described another syndrome of acute postemetic lacerations of the gastric cardia as a source of major haemorrhage following an alcoholic debauch. The decision for surgical or non-surgical management of oesophageal perforation from any aetiology remains difficult.

Because perforations occur during oesophagoscopy, gastroscopy, and oesophageal dilatation, frequent contemporary use of upper gastrointestinal fibreoptic endoscopy has increased the actual number of perforations. The most common area of perforation from an endoscopic examination is the region of the cricopharyngeus muscle. The perforation rate of 0.11 per cent in a 1988 survey of 35412 endoscopic examinations is unchanged by comparison with the 0.13 per cent rate reported in a 1974 survey of 211 410 endoscopic examinations.

Dilatation of the oesophagus carries a risk of perforation because it is usually performed for relief of stricture resulting from reflux oesophagitis, postoperative stenosis, or achalasia. Even bouginage under endoscopic control gives a false sense of security, as perforation can occur without the operator's knowledge when the bougie is pushed ahead of the endoscope. Early dilatation after a caustic burn may also predispose to perforation because it is performed through friable tissues.

Forceful hydrostatic or pneumatic dilatation for achalasia carries a 4 per cent incidence of oesophageal perforation with mediastinal sepsis versus only a 1 per cent incidence after oesophagomyotomy. Dilatation with semiflexible bougies (Eder–Puestow or Savary type bougies), which have a hollow centre and can be threaded on to an endoscopically inserted guide wire, or with mercury filled bougies is even less dangerous (<0.5 per cent) and does not have to be performed under fluoroscopy. To obtain an upper gastrointestinal series before endoscopy or dilatation is, however, a wise step if the patient has an history of dysphagia, regurgitation, reflux oesophagitis, or previous oesophageal surgery.

Celestin plastic tubes passed transorally through an unresectable carcinoma of the oesophagus as a palliative procedure have also been incriminated in iatrogenic perforation. Sengstaken–Blakemore tubes and Linton tubes for tamponade of oesophageal varices can cause oesophageal disruption when they are kept inflated too long or when an agitated patient extracts them while they are still inflated. Oesophageal perforation occurs also after sclerotherapy (either by puncture of needle or necrosis from sclerosant) for variceal haemorrhage, and endoscopic laser therapy of advanced oesophageal carcinomas.

Traumatic endotracheal intubation usually perforates the oesophagus just below the cricopharyngeus muscle, generally in the dorsal midline at an area of weakness where the mucosa is supported only by fascia (Lannier's triangle). Para-oesophageal operations such as hiatal hernia repair, vagotomy, and radical pneumonectomy are also responsible for oesophageal perforation. Simple monitoring devices such as the oesophageal stethoscope or the oesophageal obturator airway included in some cardiopulmonary resuscitation kits have caused oesophageal perforation.

Patients with postemetic spontaneous perforations of the oesophagus are properly classified as examples of Boerhaave's syndrome. The adjective ‘spontaneous’ does not imply the absence of predisposing factors or of underlying oesophageal disease; rather this term means perforation not resulting from iatrogenic trauma, foreign body, or direct external trauma. Spontaneous rupture of the oesophagus and acute postemetic lacerations of the gastric cardia (Mallory–Weiss syndrome) are probably related, since vomiting causes both syndromes. The precise physical and clinical conditions that are prerequisites for rupture or laceration are often unknown, however. Perhaps the lack of muscularis mucosa in the wall of the lower oesophagus may be one anatomical explanation.

Jackson and Jackson reported the classic account of 2733 foreign bodies lodged in the oesophagus; of these 526 were bones and 535 coins. The frequency of bones is not surprising as they can be present in food. In adults, the wearing of artificial dentures may inhibit feeling an object before swallowing and can be the indirect cause of swallowing or inhaling a foreign body. Pieces of artificial denture may also be swallowed. Endoscopic removal of the foreign body should be performed under general anaesthesia, especially in the paediatric age group. Severe perforations can be caused by attempted removal of foreign bodies, either by a poorly trained endoscopist or by one who tries to push the foreign body ahead of the endoscope into the stomach too vigorously. Whenever possible, a duplicate of the foreign body should be obtained in order to select accurately the proper endoscope and forceps to use. The duplicate can also afford an opportunity to study possible presentations of the object in the oesophageal lumen. Considering the elasticity of a normal oesophagus, the surgeon faced with impaction of a smooth foreign body should suspect a pre-existing oesophageal stricture.

Because of the protected location of the oesophagus, penetrating injuries are rare and are generally associated with injuries to other surrounding structures. In a 1979 review of 125 consecutive penetrating wounds of the chest (54 per cent stab wounds and 46 per cent gunshot wounds) oesophageal perforation was disclosed at early thoracotomy in only three cases. Reference to earlier series shows that penetrating wounds of the thoracic oesophagus carry a mortality of 47 to 57 per cent compared with 11 to 17 per cent for cervical oesophageal wounds.

Although 7 per cent of patients may be asymptomatic, oesophageal perforation usually causes severe thoracic pain, followed by fever, dysphagia, mediastinal and subcutaneous emphysema, and ultimately dyspnoea and systemic sepsis. Shock and empyema are more frequent after perforation of the thoracic oesophagus than after perforation of the cervical oesophagus. The presence of one or several of these symptoms or signs after clinical events such as oesophagogastric endoscopy, instrumentation, or insertion of tubes should lead to early diagnosis of oesophageal perforation (or at least to early suspicion of such a diagnosis).

As a rule, preoperative confirmatory evidence of oesophageal perforation should be obtained by chest radiography and a Gastrografin (meglucamine ditrizoate) swallow study, followed eventually by barium study if the Gastrografin swallow is negative. Computed tomographic scan of the mediastinum after contrast swallow is sometimes useful to visualize a tiny oesophageal perforation that has been missed by conventional radiographic study. A radiograph of the cervical spine is helpful in some patients suspected of having perforation of the cervical oesophagus. Air is often evident in the prevertebral tissue planes. A widened retropharyngeal space seen on a lateral cervical radiography (Fig. 1) 885 or a computed tomographic scan (Fig. 2) 886 due to an abcess, gives a definitive answer. The disappearance of normal cervical spinal lordosis and appreciable anterior displacement of the oesophagus and the upper airways are other useful diagnostic elements.

To localize a radio-opaque foreign body, radiographs of the neck (anteroposterior and lateral views) should be made in hyperextension, since the normal position of the clavicular shadow hides the oesophageal inlet. Hyperextension of the neck raises the larynx and the oesophageal inlet, making them visible in the lateral projection. If the suspected object is not radio-opaque (the pull-tab of a drinks can is a frequent example in children), a contrast examination with thin barium solution is also indicated.

Widening of the superior mediastinum, cervical subcutaneous emphysema in a patient with a neck wound, and increased distance between the trachea and the vertebrae (prevertebral shadow) are the main radiographic signs of traumatic cervical oesophageal perforation. Widening of the entire mediastinum, mediastinal emphysema, and hydropneumothorax are the most common findings in thoracic oesophageal perforation (either iatrogenic or spontaneous). All patients who are seen with haematemesis or bloody drainage from the nasogastric tube following trauma to the chest should be studied promptly with Gastrografin oesophagography to ascertain the presence of perforation. All cervical wounds penetrating the platysma muscle should be explored to rule out oesophageal injury or injury to other cervical structures.

Five modes of treatment are proposed: non-operative conservative treatment, drainage alone, suture repair of the perforation (supported or not by local tissue flap), early oesophagectomy, and oesophageal exclusion.

The non-operative approach can be attempted early after instrumental perforation occurring in a hospital environment with a patient in fasting conditions who has minimal systemic symptoms and no evidence of clinical sepsis. Such a conservative treatment includes massive antibiotic therapy (against aerobic and anaerobic bacteria), intravenous hydration, withdrawal of all oral intake, and eventually nasogastric drainage and total parenteral nutrition. However, in the early stage after an instrumental perforation of the cervical or thoracic oesophagus it is impossible to determine whether a tiny transmural perforation will lead to massive pleural contamination with subsequent shock and adult respiratory distress syndrome (or will remain contained within the mediastinum).

Absolute indications for emergency operation are the presence of hydropneumothorax, pneumoperitoneum, empyema, systemic sepsis, shock, and adult respiratory distress syndrome. The surgical option (drainage alone, suture repair, oesophagectomy, oesophageal exclusion) depends on the site of injury (cervical, thoracic, or abdominal).

Suture and drainage by placement of Penrose or Jackson–Pratt drains are performed through an incision anterior to the sternocleidomastoid muscle.

Simple pleural drainage or drainage through a paravertebral rib resection is sometimes indicated for the poorest surgical risks (elderly patients with several complicating factors, physical status corresponding to classes 4 and 5 in the classification of the American Society of Anesthesiologists). The mortality rate after simple drainage is 50 per cent; even in these difficult situations, we recommend early thoracotomy and closure of the perforation. However, releakage following suture repair continues to be the principal cause of postoperative morbidity and mortality. The degree of inflammatory change in the muscular wall of the oesophagus is such that layered closure may be impossible or technically unsatisfactory, especially when the diagnosis has been delayed. For this reason, the suture should be supported with a local tissue flap, including pericardium, diaphragm, intercostal muscles, and gastric wall (Fig. 3) 887.

Another simple way of dealing with the problem of delayed recognition of oesophageal perforation consists of flapping or wrapping a pedicled pleural flap (Fig. 4) 888 on or around the oesophagus, suturing it firmly over the area of leakage and around its margin. This procedure has the virtue of permitting closure of the perforation and complete cleansing of the pleural space, with decortication of exudate from the lung surface and avoidance of a second operation. Drainage gastrostomy and sometimes feeding jejunostomy are performed concurrently.

Early oesophagectomy followed by re-establishment of gastrointestinal continuity by a left colon bypass or oesophagogastrostomy is indicated in the presence of obstructing lesions of the thoracic oesophagus (such as cancer, caustic burn with stricture, severe stricture related to hiatal hernia with reflux). In these situations, it is better to resect both the perforation and the original lesions, rather than to rely on repair and drainage alone. Oesophagectomy should be performed within a few hours after perforation: greater delay, and the presence of local and systemic infection, requires the resection to be made in badly contaminated tissues with potential risks to the anastomosis.

Exclusion–diversion of the oesophagus, when the diagnosis has been delayed or the primary treatment has failed, is the only way to control persistent mediastinal and pleural infection. The principle underlying exclusion–diversion has long been applied to the treatment of fistulae of other portions of the intestinal tract. For perforation of the thoracic oesophagus, the technique consists of suturing the oesophageal perforation, instituting mediastinal and pleural drainage, and placing an umbilical tape or a large ligature around the oesophagus above the cardia and deep to the vagus nerves. Temporary oesophageal exclusion using the stapling technique has also been described; a cartridge of the TA 55 stapler is applied to the oesophageal wall just above the cardia. Repermeation of the oesophagus can occur within 30 days following stapling.

Diversion of the upper oesophagus is then accomplished by cervical oesophagostomy. A gastrostomy is performed for feeding. At a time of election after healing of the perforation, a thoracotomy is performed and the oesophageal ligature above the cardia is removed. The cervical oesophagostomy is also closed.

Perforation of the abdominal portion of the oesophagus generally occurs after vagotomy or hiatal hernia repair, and can be treated by primary suture repair and drainage of the upper abdomen. The suture of the perforation can be supported with a local tissue flap made of stomach wall (Fig. 3) 887 as recommended for thoracic perforation.

Patients who present with upper gastrointestinal bleeding and have a recent history of vomiting or retching, especially when associated with recent alcohol intake, should be endoscopically examined for presence of lacerations of the gastric cardia or the gastro-oesophageal junction, which are indicative of the Mallory–Weiss syndrome. Emergency endoscopic examination is mandatory in order to locate the site of bleeding accurately and assess its severity. Endoscopy will also reveal other synchronous upper gastrointestinal lesions, and will help direct the surgeon to the responsible lesion should a surgical procedure be required to control the haemorrhage.

Bleeding from Mallory–Weiss lacerations is controllable by non-operative therapy in the majority of these patients. Resuscitative measures that should be carried out before and during the emergency endoscopic procedures include immediate assessment of the clinical and haemodynamic status, maintenance of intravascular volume, and gavage with ice water using a No. 36 F Ewald&subR; tube. In many instances, bleeding from Mallory–Weiss lacerations is so minor that gavage with ice water controls the bleeding.

Balloon tamponade for the treatment of Mallory–Weiss syndrome is contraindicated, since the inflated balloon may cause tears in a gastric hiatal hernia, which is commonly found in patients with Mallory–Weiss Syndrome.

Ten units of vasopressin diluted in 10 ml of saline solution injected intravenously over a 10-min period will induce vasoconstriction if no coronary artery disease is evident. The vasopressin injection can be repeated at intervals of 1 to 2 h, or (preferably) a constant intravenous infusion of 0.3 to 0.4 units per minute can be started. However haemodynamic function and urine output must be monitored carefully, since tachyphylaxis and an antidiuretic effect can develop.

Indications for the surgical treatment of Mallory–Weiss syndrome are decreasing, and no definite study has demonstrated the value of one surgical procedure over another. The surgical technique generally used to control massive bleeding from a Mallory–Weiss laceration that remains refractory to all conservative measures is oversewing the lacerations with a running suture of 2–0 catgut through an anterior gastrotomy (Fig. 5) 889. The best exposure is obtained through gastrostomy made in the middle one-third of the stomach and by using a large Deaver retractor while pulling upward on the nasogastric tube. This allows the cardia to be brought into view and exposes the folds at the oesophagogastric junction.

For lacerations that extend higher into the lower oesophagus, left thoracotomy may be necessary to expose the bleeding tears by opening the oesophagus. If unremitting haemorrhage from associated gastritis complicates the situation, truncal vagotomy should be coupled with a generous gastrectomy.

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