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Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Esophageal Rupture Emesis leading to a fatal rupture of the esophagus was described by Herman Boerhaave (1668–1738) in 1724. Hematemesis due to post-emetic mucosal laceration of the lower end of the esophagus and gastric cardia was recognized by Boston pathologist, Kenneth G. Mallory (b 1900) and American physician, Konrad Weiss (1898–1942) in 1929. See Boerhaave syndrome.
Test Paper 7
Published in Teck Yew Chin, Susan Cheng Shelmerdine, Akash Ganguly, Chinedum Anosike, Get Through, 2017
Teck Yew Chin, Susan Cheng Shelmerdine, Akash Ganguly, Chinedum Anosike
Non-accidental abdominal trauma is the second leading cause of death from child abuse after head trauma. Presentation is usually delayed with abdominal pain, vomiting, peritonism and signs of obstruction. Non-accidental visceral trauma is more common in the age group presented here than is incidental blunt abdominal injury and should always be considered as a differential diagnosis, especially if there are other associated features of NAI. Visceral perforation/laceration, intramural haematoma and shocked bowel syndrome are all within the spectrum of NAI. Boerhaave syndrome is a complete transmural oesophageal rupture caused by forceful vomiting or impacted food bolus and more commonly affects adults.
Gastrointestinal and Genitourinary Imaging
Published in Gareth Lewis, Hiten Patel, Sachin Modi, Shahid Hussain, On Call Radiology, 2015
Gareth Lewis, Hiten Patel, Sachin Modi, Shahid Hussain
Oesophageal perforation is most commonly iatrogenic in nature and can be seen secondary to endoscopy, oesophageal dilation, myotomy and stent placement, foreign body extraction, gastric fundoplication and anterior cervical discectomy. Perforation can also occur secondary to tumours and severe ulceration resulting from gastro-oesophageal reflux disease. Spontaneous oesophageal rupture, termed Boerhaave syndrome, is usually associated with vomiting. It is believed that incomplete cricopharyngeal muscle relaxation during vomiting results in a sudden increase in oesophageal intraluminal pressure, which can result in perforation. This should be distinguished from a Mallory-Weiss tear, which is also associated with protracted vomiting but is not transmural and therefore does not result in oesophageal perforation. The most common site of spontaneous perforation is the thoracic oesophagus, particularly the distal left posterior wall. Symptoms and signs include sudden onset chest pain, haematemesis and fever. Blood tests may show raised inflammatory markers or, alternatively, may be normal. Oesophageal perforation has a high mortality rate and early diagnosis and surgical intervention is vital.
Outcomes after hybrid minimally invasive treatment of Boerhaave syndrome: a single-institution experience
Published in Acta Chirurgica Belgica, 2023
Stefanie Willems, Jean H. T. Daemen, Karel W. E. Hulsewé, Eric H. J. Belgers, Meindert N. Sosef, Khalida Soufidi, Yvonne L. J. Vissers, Erik R. de Loos
Boerhaave syndrome or spontaneous esophageal rupture is typically caused by forceful emesis and is considered to be a medical emergency [1]. The clinical presentation of this syndrome is diverse, prompting a challenge for its diagnosis. The typical triad of symptoms, also known as Mackler’s triad, includes acute chest pain, vomiting and subcutaneous emphysema. However, patients may also present with less discriminative symptoms depending on the level of perforation and the degree of contamination [2]. Rapid diagnosis and intervention are critical since Boerhaave syndrome is a rare cause of gastrointestinal perforations, but amongst the most lethal with a mortality rate up to 40% when treatment is delayed for over 24 h after rupture [3]. Diagnostic delay and continuous spill of bacteria and digestive enzymes to the mediastinum can lead to severe mediastinitis, empyema and septic shock [4].
Outcome after stenting and débridement for spontaneous esophageal rupture
Published in Scandinavian Journal of Gastroenterology, 2018
Tobias Hauge, Ole Christian Kleven, Egil Johnson, Bjørn Hofstad, Hans-Olaf Johannessen
Spontaneous postemetic rupture of the esophagus (Boerhaave syndrome) is a devastating event with high morbidity and mortality, mainly because of diagnostic delay and irreversible gastric contamination of the mediastinum and pleural cavities. Surgery has been the main-stay of the treatment [1], including primary repair, resection or exclusion of the perforation combined with drainage and débridement of the contaminated chest. During the past 15 years, sealing of the perforation by placement of a self-expanding metal stent (SEMS) has increasingly been used [2,3] with promising results. The main goals of stent-based treatment are to seal and close the perforation effectively, to drain all fluid collections in the pleura and the mediastinum, primarily percutaneously, and perform surgical débridement in selected patients. In the situation of a clearly contaminated and turbid pleural effusion that may contain food remnants, surgical débridement of the chest is mandatory in order to avoid a potentially fatal outcome.
Pneumomediastinum in late pregnancy: a case report and review of the literature
Published in Acta Chirurgica Belgica, 2023
N. Zonnebeld, P. P. H. L. Broos, S. M. E. Engelen, Y. L. J. Vissers, E. R. de Loos
Boerhaave syndrome is a rare (i.e. <10%) ‘spontaneous’ rupture of the esophagus, and was first described by Boerhaave in 1724 [11]. Presumably the pathophysiological mechanism is a rupture of the lower third of the esophagus due to an intra-esophageal pressure rise caused by a failed relaxation of the upper esophageal sphincter during vomiting. Consequently, gastric content can rupture the esophagus.