Transition of a Mallory-Weiss syndrome to a Boerhaave syndrome confirmed by anamnestic, necroscopic, and autopsy data: A case report

Abstract

Rationale: Spontaneous esophageal rupture (Boerhaave syndrome) is a rare, though frequently fatal, event. It is generally caused by a sudden increase in pressure inside the esophagus. In some cases, full-thickness perforations of the esophagus may develop from previous lesions that initially involve only the esophageal mucosa (Mallory-Weiss syndrome) and which, following further triggering events, give rise to a transmural lesion.

Patient concerns: Here, we present the case of a 45-year-old subject who suddenly died of acute cardio-respiratory failure, an autopsy was performed to identify the cause of death.

Diagnosis, interventions, and outcomes: The autopsy examination revealed a full-thickness rupture of the esophageal wall. Through the integration of necroscopy findings, anamnestic data, and histopathological examination, it has been possible to establish that complete esophageal rupture resulted from the evolution of a previous partial lesion of the esophageal wall, and that an untreated Mallory-Weiss syndrome evolved into a rapidly fatal Boerhaave syndrome.

Lessons: This case shows that distal esophageal tears, rather than constituting a distinct entity, may be part of a spectrum of diseases and that a partial lesion of the esophageal wall caused by barogenic injury may evolve into a full-thickness rupture following further barotraumas.

Figure 1

(A) Bilateral pleural effusion of brownish material. (B) Three centimeter esophageal tear in the right lateral wall of the inferior third. (C) Intestinal hemorrhage. (D) Marked hepatic steatosis.

Figure 2

(A, B) Neutrophil infiltration of the esophageal mucosa and submucosa (H&E 40×), (H&E 4×). (C, D) Digested material and the presence of hemosiderin accumulations in the esophageal mucosa and submucosa (Perls 60×).