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We would like to report a fatal case of post-emetic oesophageal perforation (Boerhaave’s syndrome). The condition was attributed to nausea and retching caused by raised intraocular pressure (IOP). We believe the case highlights the importance of early diagnosis and management of such rare cases.
An 81 year old man presented with a painful right eye. He felt nauseated and was retching. On examination visual acuity was 6/36 pinhole 6/18 right eye and 6/12 pinhole 6/5 left eye. The right eye was mildly inflamed and pseudophakic as a result of recent surgery. Right IOP was 58 mm Hg. The left eye showed no abnormality. Past ocular history included complicated right cataract surgery requiring pars plana vitrectomy and removal of lens fragment 6 weeks previously. Five weeks later he developed an inferior retinal detachment which was repaired by further vitrectomy, cryotherapy, encircling band, and gas tamponade (SF6 20%). Following discharge he had been troubled by nausea and retching. Past medical history included moderate chronic obstructive pulmonary disease and treated essential hypertension. Medical examination was consistent with this. He was admitted and treated with intravenous Diamox and Maxolon, topical Alphagan and Trusopt. IOP was 33 mm Hg 5 hours later. Early the following morning he had one episode of blood stained vomitus following which he developed sudden retrosternal chest pain and dyspnoea. GTN spray and Gaviscon did not alleviate his symptoms. On examination he was very distressed and unable to lie flat. Cardiovascular and respiratory examination demonstrated no new pathology. His blood pressure, ECG, and oxygen saturation were normal. Abdominal examination revealed general tenderness and guarding in all quadrants. Abdominal and chest x rays were unremarkable as was abdominal ultrasound. Urgent surgical and medical opinions were sought. At lunch time he developed further sudden severe dyspnoea and became confused. Blood gases revealed severe acidosis with reduced Po2 and Pco2. Physicians believed this was a mixed metabolic and respiratory acidosis induced by pulmonary thromboembolism. He was anticoagulated and transferred to the high dependency unit. Repeat chest x ray at 20:00 showed a right sided pneumothorax. A chest drain was inserted. The pleuritic fluid sample contained bile, Gram positive cocci, and Gram negative rods. The patient, who by now was in septic shock, was commenced on broad spectrum intravenous antibiotics. Emergency laparotomy confirmed oesophageal perforation. After discussion with his family no further intervention was deemed justifiable. Our patient died a few hours later.
Boerhaave syndrome is transmural perforation of the oesophagus to be distinguished from Mallory-Weiss syndrome, non-transmural oesophageal tear also associated with vomiting.1 It is the result of a sudden rise in intraluminal oesophageal pressure produced during vomiting. Pain is the most consistent symptom, present in 70–90% of patients, and is usually related to the site of disruption (Table 1).2 Chest x ray suggests the diagnosis in 90% of patients, but immediately after disruption the chest film may be normal.3 Pneumomediastinum, surgical emphysema, mediastinal widening, or a mediastinal air-fluid level must prompt investigation to rule out oesophageal perforation.4 Survival depends upon early recognition and appropriate surgical intervention. The overall mortality rate is approximately 35%. Surgical repair within 24 hours carries 70–75% chance of survival. This falls to 35–50% if surgery is delayed longer than 24 hours and to approximately 10% if delayed longer than 48 hours.5 Surgical intervention is the optimum management in most cases.6 This case highlights two very important points, firstly, the importance of adequate IOP control and associated nausea, secondly, although the above case is rare familiarity of the case and its inclusion in the differential diagnosis can be potentially life saving.