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J Thorac Cardiovasc Surg 2003;125:976
© 2003 The American Association for Thoracic Surgery
Letters to the Editor |
Massachusetts General Hospital, Boston, MA 02114
To the Editor:
I read with interest the case of a patient with acute leukemia and segmental esophageal necrosis reported by Salo and associates.
1 The authors imply that intussusception led to ischemia, and circumferential full-thickness loss of the esophagus was repaired "without interruption." Both assumptions may be challenged. The patient had no risk factor for gastroesophageal intussusception,
2 in which stomach is the intussusceptum, not esophagus, and perforation, rather than necrosis, a reported complication. Fungal infection of the esophagus in leukemia, however, is known to result in full-thickness necrosis and esophageal expulsion.
3 Their final comment relating to Aspergillus infection of the esophageal wall points to the likely cause of necrosis.
A complete loss of all esophageal layers, no matter how short, is expected to result in cicatricial stricture that may have been delayed in this case by cytotoxic therapy. Indeed, dysphagia later developed, necessitating further intervention. The mediastinal soft tissues may resemble the esophageal lumen so that perforation is not obvious. However, bare of epithelium and exposed to esophageal contents, the mediastinum provides an entry to systemic infection, particularly in an immunosuppressed state. Esophageal resection with immediate or delayed reconstruction should be considered even in this patient population to prevent mediastinitis and restore swallowing.
References
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