Short reportsFood embolus1
Introduction
Stroke prevention requires the anticipation and treatment of both typical and atypical emboli. Air, fat, bacterial aggregates and food are all known causes of stroke and treatment strategies vary accordingly. Of these, food emboli are the rarest and they arise solely from esophago-atrial fistulas (Prolla et al., 1967, Hojgaard and Raaschou-Nielsen, 1970, Laubscher, 1970, Itabashi and Granada, 1972, Strong, 1974, Mott and Austin, 1976, Cunnane, 1978, Murphy et al., 1979, Nadjmi et al., 1979, Sumithran et al., 1979, Brynjolfsson et al., 1980, Flodmark, 1983, Maurange et al., 1983, Lambert et al., 1987, Snyder et al., 1990, Miller et al., 1991). Such lesions are invariably fatal, causing either exsanguination or embolization. We describe a patient with food emboli from an esophagoatrial fistula and suggest, based on a review of the literature, a possible means of early recognition and treatment.
Section snippets
Case report
A 74 year old man with a long history of dysphagia, esophagitis, esophageal diverticulum and esophageal stricture treated with dilation, developed flu-like symptoms of fever, congestion, vomiting and dizziness. He was examined in an emergency department, treated with Cefixime, and discharged with a presumed upper respiratory infection. He returned with worsening symptoms three days later. While standing for an orthostatic assessment of blood pressure, he abruptly lost consciousness and
Autopsy
Post-mortem examination revealed a 6×6×3 cm diverticulum midway along the course of the esophagus filled with approximately 30 ml of partially digested food. The diverticulum was adherent to the left atrial surface and a 1×0.8 cm. fistula connected the diverticulum with the left atrium (see Fig. 1). Approximately 5 ml of food debris was in the left atrium and a smaller amount in the left ventricle from whence food debris had embolized to virtually every organ system, including the heart, liver,
Discussion
Our patient's multiple risk factors of esophageal inflammation, stricture, dilation and diverticulum most likely contributed to his development of a chronic fistula (Prolla et al., 1967, Hojgaard and Raaschou-Nielsen, 1970, Laubscher, 1970, Itabashi and Granada, 1972, Strong, 1974, Mott and Austin, 1976, Cunnane, 1978, Murphy et al., 1979, Nadjmi et al., 1979, Sumithran et al., 1979, Brynjolfsson et al., 1980, Flodmark, 1983, Maurange et al., 1983, Lambert et al., 1987, Snyder et al., 1990,
Acknowledgements
The authors thank Susan Huff for her editorial review and comments.
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Presented in part at the 46th Annual American Academy of Neurology Meeting, Washington, DC, May, 1994.