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Oesophageal
rupture and perforation
Causes
Spontaneous
- raised intraoesophageal pressure
- oesophageal CA
- peptic ulceration
Traumatic
- penetrating chest trauma
- blunt trauma
- foreign body
- swallowed caustic agents
Iatrogenic
Instrumentation
- dilatation
- oesophagoscopy
- intubation
Surgery
- anastamotic leak
- intraoperative:
- vagotomy
- thyroidectomy
- oesophageal myotomy
- aortic surgery
Clinical features
- often produces immediate and often catastrophic clinical features
- perforation due to direct trauma from endoscope occurs most commonly in
cervical region: early signs include neck pain or stiffness, difficulty
swallowing, cough and cervical emphysema. Patient may not develop signs of
serious illness for several hours due to discontinuity between cervical
oesophagus and mediastinum
- perforation of intrathoracic oesophagus generally results in more rapid
progression to acute illness due to quick spread of infection, rapid
development of mediastinitis and fluid sequestration
- chest pain within minutes
- dyspnoea frequently prominent
- pleural effusion
- mid oesophageal perforations (common when secondary to dilatation)
associated with spread into right pleural cavity, lower oesophageal
perforations (common in spontaneous perforations) associated with spread into
left pleural cavity
- intra-abdominal perforation causes peritonitis, systemic sepsis and
epigastric pain within mins-hours
Investigations
CXR:
- pleural effusion
- pneumomediastinum
- gastrograffin swallow
- food particles, pH<6 and amylase in pleural
fluid
- CT may be useful if diagnosis remains in doubt, especially if there is a
delay in diagnosis
Management
- usually surgical, ± primary closure
- broad spectrum antibiotic cover including anaerobic cover
- criteria for attempting non-operative management:
- early diagnosis, or if diagnosis is late there should be evidence that
infection is walled off
- infected cavity should be well drained with minimal intrathoracic soilage
- no intake of food between time of injury and time of diagnosis
- no distal obstruction by tumor or stricture
- no clinical manifestations of acute illness (eg fever, severe pain)
- no signs of sepsis or other significant physiologic derangements
- non-operative managment generally includes:
- NG drainage
- chest drainage on side of perforation
- broad spectrum antibiotics
- TPN for at least 10 days, nil by mouth
- if patient’s condition deteriorates or fails to improve in 24 h seriously
reconsider operative management
Outcome
- factors associated with poor outcome:
- poor general condition, especially associated oesophageal CA
- spontaneous worse than traumatic or instrumental
- intrathoracic or intra-abdominal
- >24 h delay in diagnosis and initiation of treatment
- mortality averages ~15%
Spontaneous rupture
- most commonly follows forceful vomiting but has been reported following
defaecation, childbirth, blunt trauma, fits, heavy lifting and forceful
swallowing
- elevated amylase in pleural fluid strongly suggests diagnosis but its
absence does not exclude it. Raised pleural fluid amylase, epigastric pain,
nausea and vomiting can also be due to acute pancreatitis
- Mackler's triad (vomiting, chest pain and cervical emphysema) almost
pathognomonic but absent in almost half the cases
- most spontaneous perforations occur in lower left oesophagus just above
diaphragm
- definitive diagnostic test is gastrograffin swallow
- virtually all cases require surgery
Further reading
Sellke FW. Esophageal perforation and mediastinitis. In Rippe JM, Irwin RS,
Fink MP, Cerra FB (eds), Intensive Care Medicine, 3rd ed. Little Brown &
Co., Boston, 1996, pp 1841-5
© Charles Gomersall December 1999
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