Atraumatic so-called “spontaneous” rupture of the esophagus

Abbott, Osier A.; Mansour, Kamal A.; Logan, William D.; Hatcher, Charles R.; Symbas, Panagiotis N.

doi:10.1016/s0022-5223(19)42515-4

Cited by 216 publications

(21 citation statements)

References 26 publications

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“…Delayed diagnosis is sometimes fatal because late operation tends to result in anastomotic leakage. Despite numerous reports documenting potential treatments for esophageal rupture in cases of delayed diagnosis [including diversion and exclusion, and establishment of a controlled fistula (T‐tube), Atkinson tube and non‐surgical management], 11 –15 these are still controversial. We have described an effective method of treatment for the spontaneous rupture of the esophagus using a covered self‐expanding metallic stent.…”

Section: Discussionmentioning

confidence: 99%

Covered metallic stent treatment of a patient with spontaneous rupture of the esophagus

Tsunoda

Shimada

Watanabe

et al. 2001

Diseases of the Esophagus

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A patient with a potentially fatal condition as a result of esophago-pneumo-broncho fistula was successfully treated with the insertion of a self-expanded covered metallic stent. Severe regurgitation resulted in the removal of the stent 3 months after insertion. Stricture after removal of the stent required pneumatic balloon dilation. The use of a self-expanded covered metallic stent is effective for the treatment of spontaneous esophageal rupture; however, early removal of the stent is recommended.

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Section: Discussionmentioning

confidence: 99%

Covered metallic stent treatment of a patient with spontaneous rupture of the esophagus

Tsunoda

Shimada

Watanabe

et al. 2001

Diseases of the Esophagus

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“…The tear usually occurs vertically on the left posterolateral part of the distal oesophagus, presumably because this area is weaker and is first to give way when the intra‐oesophageal pressure is raised [1]. In our patient, however, the leak occurred on the right, which has been reported rarely [2, 4], except in the series of W alker et al [5], in which the incidence was equal on both sides. This could be caused by a diseased oesophagus, as suggested by the presence of a diverticulum seen on endoscopy 6 yrs previously.…”

Section: Discussionmentioning

confidence: 56%

“…He had also shown endoscopic evidence of duodenitis 6 yrs previously, and this may be a contributory factor to the symptoms. Peptic ulcer disease is known to occur in some patients with Boerhaave′s syndrome [2, 3]. Complete endoscopic evaluation was not possible in our case because of the development of an oesophageal stricture, but contrast studies did not show evidence of peptic ulceration.…”

Section: Discussionmentioning

confidence: 68%

“…Spontaneous (atraumatic) rupture of the oesophagus after forceful vomiting is also termed Boerhaave′s syndrome, after the person who first described it in 1724 [1]. It is of rare occurrence, and case reports and a few retrospective case series represent the majority of publications in this area [2–5].…”

Section: Discussionmentioning

confidence: 99%

“…Other diagnostic modalities include computed tomography or pleural fluid analysis of food content and pH. A bbott et al [2] described the character of the pleural fluid, which appears serous or serosanguineous prior to rupture of the mediastinal pleura and changes to brown or rusty brown following the rupture. They considered the latter to be a clue to the diagnosis and that failure to appreciate this led to diagnostic delay in their series.…”

Section: Discussionmentioning

confidence: 99%

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“Coffee grounds” through the chest tube

Al-Mobeireek¹,

Alkattan²

2000

Eur Respir J

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A 78-yr-old Saudi male was admitted having had epigastric pain and vomiting for 3 days. The patient was unable to give a clear medical history; however, he described the pain to be severe, colicky, nonradiating and aggravated by food. On the day of admission, he had noticed a small amount of fresh blood in the vomitus. The family indicated that he had had a long-standing history of intermittent abdominal pain, mainly related to food, for the past 25 yrs. Indeed, he had been admitted to the surgical ward 6 yrs previously with similar pain and was suspected to have a perforated duodenal ulcer, but recovered with conservative treatment. A few weeks after discharge he underwent upper gastrointestinal endoscopy, which showed oesophageal and duodenal diverticula and duodenitis. He was treated with ranitidine for 6 weeks with improvement and did not attend any further follow-up until this presentation. The physical examination results were unremarkable apart from pallor and epigastric tenderness.The haemogram was consistent with severe microcytic hypochromic anaemia. Serum electrolytes, urea, creatinine, amylase and random blood glucose levels were within the normal range. The initial chest radiograph is shown in figure 1. The following morning, the physician on duty was called to see him owing to severe respiratory distress. Examination of the chest showed dull percussion notes on both lung bases and numerous crackles. The chest radiograph showed large bilateral pleural effusions and a rightsided apical pneumothorax. Chest tubes were inserted and drained rusty brown fluid with clots (coffee groundslike).

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