Boerhaave Syndrom: an unusual complication of acute vomiting in a child
Details
Serval ID
serval:BIB_441C3D1BA893
Type
Inproceedings: an article in a conference proceedings.
Publication sub-type
Poster: Summary – with images – on one page of the results of a researche project. The summaries of the poster must be entered in "Abstract" and not "Poster".
Collection
Publications
Institution
Title
Boerhaave Syndrom: an unusual complication of acute vomiting in a child
Title of the conference
Joint Annual Meeting of the Swiss Society for Pediatrics, Swiss Society of Pediatric Pneumology
Address
Crans Montana, Switzerland, June 17-18, 2010
ISBN
1424-7860
Publication state
Published
Issued date
2010
Peer-reviewed
Oui
Volume
140
Series
Swiss Medical Weekly
Pages
9S-10S
Language
english
Notes
Meeting Abstract
Abstract
Introduction: Boerhaave syndrome (BS) is a spontaneous
esophageal perforation, described in aged, alcoholic males, secondary
to forceful vomiting. BS has rarely been described in children.
Case presentation: The patient is a 7-year-old Nigerian girl. She has
a past history of clinical gastro-esophageal reflux (treated
conservatively with prokinetics and good evolution), malaria at the age
of 3 months and an episode of acute pancreatitis at 5 years. One week
prior admission, she had stopped atovaquone-proguanil (AP)
prophylaxis after a trip in an endemic area. Two days prior admission,
she presented several bouts of isolated acute vomiting, without fever
or diarrhea. On admission, she complained of chest pain. Cardiac
auscultation revealed crepitus. No subcutaneous emphysema nor
respiratory distress was present. Chest radiography and CT-scan
confirmed a pneumomediastinum extending to the neck. Esophageal
perforation was suspected. An upper gastrointestinal endoscopy was
performed and showed a small esophageal tear, grade II-III
esophagitis and a single gastric ulcer without any sign of H. Pylori
infection. Enteral feeds were stopped and a nasogastric sucking tube
inserted. The patient made a full recovery on intravenous antibiotics
and conservative treatment. Of note a second episode of subclinical
acute pancreatitis, treated conservatively, probably drug-induced.
Discussion: BS is a complete rupture of all layers of the esophagus,
secondary to an increased intra-abdominal pressure due to incomplete
opening of the cricophayngeal sphincter occurring during vomiting or
cough. Rarer causes include eosinophilic or Barrett's esophagitis, HIV
and caustic ingestion. Esophageal perforation in children is rare, most
of time secondary to necrotizing esophagitis in the newborn, medical
intervention (endoscopy, sucking, or intubation) or trauma in the older
child. Our patient had none of those risk factors and it is still unclear
what predisposed her to this complication. However, we believe that
preceding forceful vomiting with increased abdominal pressure acting
on a weakened oesophagus due to esophagitis might be responsible.
We could not find any association in the literature between AP and BS
nor between BS and acute pancreatitis. The origin of her recurrent
pancreatitis remains unclear, reason for which genetic testing for
mutations in the trypsinogen, trypsin inhibitor and CFTR genes will be
performed in case of a third episode.
esophageal perforation, described in aged, alcoholic males, secondary
to forceful vomiting. BS has rarely been described in children.
Case presentation: The patient is a 7-year-old Nigerian girl. She has
a past history of clinical gastro-esophageal reflux (treated
conservatively with prokinetics and good evolution), malaria at the age
of 3 months and an episode of acute pancreatitis at 5 years. One week
prior admission, she had stopped atovaquone-proguanil (AP)
prophylaxis after a trip in an endemic area. Two days prior admission,
she presented several bouts of isolated acute vomiting, without fever
or diarrhea. On admission, she complained of chest pain. Cardiac
auscultation revealed crepitus. No subcutaneous emphysema nor
respiratory distress was present. Chest radiography and CT-scan
confirmed a pneumomediastinum extending to the neck. Esophageal
perforation was suspected. An upper gastrointestinal endoscopy was
performed and showed a small esophageal tear, grade II-III
esophagitis and a single gastric ulcer without any sign of H. Pylori
infection. Enteral feeds were stopped and a nasogastric sucking tube
inserted. The patient made a full recovery on intravenous antibiotics
and conservative treatment. Of note a second episode of subclinical
acute pancreatitis, treated conservatively, probably drug-induced.
Discussion: BS is a complete rupture of all layers of the esophagus,
secondary to an increased intra-abdominal pressure due to incomplete
opening of the cricophayngeal sphincter occurring during vomiting or
cough. Rarer causes include eosinophilic or Barrett's esophagitis, HIV
and caustic ingestion. Esophageal perforation in children is rare, most
of time secondary to necrotizing esophagitis in the newborn, medical
intervention (endoscopy, sucking, or intubation) or trauma in the older
child. Our patient had none of those risk factors and it is still unclear
what predisposed her to this complication. However, we believe that
preceding forceful vomiting with increased abdominal pressure acting
on a weakened oesophagus due to esophagitis might be responsible.
We could not find any association in the literature between AP and BS
nor between BS and acute pancreatitis. The origin of her recurrent
pancreatitis remains unclear, reason for which genetic testing for
mutations in the trypsinogen, trypsin inhibitor and CFTR genes will be
performed in case of a third episode.
Web of science
Create date
08/09/2010 13:45
Last modification date
20/08/2019 13:48