Rupture of the Oesophagus

Introduction

This term refers to the perforation of all layers of the oesophagus and the leakage of air and ingesta into the surrounding tissues. The contents of the oesophagus are not sterile and bacteria are seeded into surrounding tissues when the oesophagus is ruptured. For most of its length, the oesophagus runs through the thoracic cavity within the mediastinum, meaning that ruptures in this location cause septic mediastinitis and pneumomediastinum. The mediastinum is continuous with the fascial planes of the neck and the spread of air and bacteria into this region leads to subcutaneous emphysema and cellulitis. It has been suggested that the spread of infection along fascial planes may be assisted by the motion of peristalsis or of pulsation in the carotid arteries. If the parietal pleural membrane (which lines the mediastinum) is also ruptured, infection and air can enter the pleural space (between the parietal and visceral pleurae), causing pyothorax and pneumothorax. If more air is drawn into the mediastinum or pleural cavity through the rupture during each inspiratory phase but not expelled during exhalation, a tension pneumothorax may develop, in which the contents of the thorax are gradually compressed by the accumulation of air. If infectious agents spread into the blood, there is a risk of systemic sepsis. Finally, if the perforation is caused by a sharp object in the region of the heart base, the great vessels arising from the heart may be lacerated causing fatal internal haemorrhage.

Perforation may occur when sharp foreign bodies become lodged in the oesophagus or when attempts are made to remove these objects endoscopically or surgically. Ruptures may also occur when anastomotic sites dehisce after oesophagectomy (as performed for the treatment of oesophageal neoplasia.)

Diagnosis

For a more complete description of oesophageal foreign bodies and their sequelae, see Oesophageal Foreign Body. The following sections refer specifically to the diagnosis and treatment of oesophageal ruptures.

Clinical Signs

These may include:

• Dyspnoea due to pleural effusion (with pyothorax), pneumothorax or tension pneumothorax.
• Subcutaneous emphysema over the neck and pectoral region.
• Pyrexia, depression, inappetence and lethargy due to infection and the acute phase response to inflammation.
• Collapse when stressed due to the absence of any respiratory reserve function, due to internal haemorrhage or to septic shock.

Diagnostic Tests

A blood haematological profile may indicate signs of severe acute inflammation, including neutrophilic leucocytosis with a right or left shift. In severe cases, a leukaemoid response (with exuberant mobilisation of neutrophils from the bone marrow storage pool) may be observed. Markers of acute inflammation (such as fibrinogen) will also be elevated.

Diagnostic Imaging

Plain radiographs of the chest may show:

• Pleural effusion with contracture of the lung lobes and presence of radiodense material around and between lobes.
• Pneumothorax or tension pneumothorax. If the latter condition is unilateral, a dorso-ventral radiograph will show that the contents of the mediastinum are pushed to one side by the expansion of the lung field on the affected side.
• Expansion of the mediastinum, best assessed on a dorso-ventral radiograph where the mediastinum will appear to be significantly wider than the vertebral column.
• Emphysema in the fascial planes of the neck.

Ultrasonography can be used to better assess the contents of the mediastinum and pleural space and to guide fine needle aspiration if samples are required.

Treatment

Animals that have developed a ruptured oesophagus have an extremely poor prognosis for survival and strong consideration should be given to euthanasia if the condition is diagnosed. If the condition is to be treated, referral to a specialist centre would be highly advisable. A possible treatment regime would include the following elements:

• Provision of oxygen by intra-nasal catheter, flow-by or mask.
• Broad spectrum intra-venous antibiosis using bactericidal drugs. Samples should be obtained from the thorax for bacterial culture and sensitivity (including anaerobic culture) and a drug that treats anaerobic bacteria should probably be used from the outset.
• Drainage of pleural effusion by thoracocentesis or, preferably, implantation of a thoracostomy tube since repeated drainage is likely to be required.
• Administration of intra-venous fluid therapy since the animal is likely to be inappetant and is likely to lose copious amounts of fluid into the exudates forming in the chest.
• Surgical repair of the rupture with repeated lavage of the pleural cavity and mediastinum when the animal is sufficiently stable.
• Provision of analgesia and intensive care monitoring in the post-operative period. If thoracostomy tubes are implanted, these can be used to lavage the pleural space with sterile saline at regular intervals.

Prognosis

Oesophageal rupture and its sequelae will be fatal in the majority of patients.

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