An unusual cause of haemoptysis: new diagnosis of an anomalous origin of the left pulmonary artery from the ascending aorta in a 20-year old man : P135
Details
Serval ID
serval:BIB_4C8FD66B7DF5
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
An unusual cause of haemoptysis: new diagnosis of an anomalous origin of the left pulmonary artery from the ascending aorta in a 20-year old man : P135
Title of the conference
Annual Joint Meeting of the Swiss Societies for Pneumology, Paediatric Pneumology, Allergology and Immunology, Thoracic Surgery
Address
Fribourg, Switzerland, April 17 and 18, 2008
ISBN
1424-3997
Publication state
Published
Issued date
2008
Peer-reviewed
Oui
Volume
38
Series
Swiss Medical Weekly
Pages
28S
Language
english
Notes
A 20-year-old man with known 22q11 microdeletion and DiGeorge
syndrome was admitted because of hemoptysis.
DiGeorge Syndrome was diagnosed six years ago with detection of a
right aortic arch, a PDA to the right pulmonary artery and an aberrant
left subclavian artery. Subsequent analyses disclosed a microdeletion
at chromosome 22q11.2.
At the most recent admission, chest CT showed an until now not
noticed anomalous origin of the left pulmonary artery (LPA) from the
ascending aorta. At cardiac catherization, a non-stenosed LPA
originating from the aorta and systemic pressure in the left lung were
documented. The right ventricle was connected to the single right PA.
Right mean PA pressure was mildly elevated at 30 mmHg. We
interpreted the hemoptysis as a consequence of pulmonary
hypertension in the left lung and suspected superinfection as
cofactor. Hemoptysis stopped spontaneously.
There is irreversible pulmonary vasculopathy in his left lung due the
anomalous origin of the LPA. Fortunately, the decrease in left lung
blood flow over time due to the progressive increase in pulmonary
artery resistance reduced the volume load on the left ventricle. The
PDA shunt flow is small and does not require intervention.
Concerning the mild pulmonary hypertension in the RPA, we
abstained from bosentan therapy because of mild symptoms and its
potential to enhance LPA blood flow and thereby left ventricular
volume load.
syndrome was admitted because of hemoptysis.
DiGeorge Syndrome was diagnosed six years ago with detection of a
right aortic arch, a PDA to the right pulmonary artery and an aberrant
left subclavian artery. Subsequent analyses disclosed a microdeletion
at chromosome 22q11.2.
At the most recent admission, chest CT showed an until now not
noticed anomalous origin of the left pulmonary artery (LPA) from the
ascending aorta. At cardiac catherization, a non-stenosed LPA
originating from the aorta and systemic pressure in the left lung were
documented. The right ventricle was connected to the single right PA.
Right mean PA pressure was mildly elevated at 30 mmHg. We
interpreted the hemoptysis as a consequence of pulmonary
hypertension in the left lung and suspected superinfection as
cofactor. Hemoptysis stopped spontaneously.
There is irreversible pulmonary vasculopathy in his left lung due the
anomalous origin of the LPA. Fortunately, the decrease in left lung
blood flow over time due to the progressive increase in pulmonary
artery resistance reduced the volume load on the left ventricle. The
PDA shunt flow is small and does not require intervention.
Concerning the mild pulmonary hypertension in the RPA, we
abstained from bosentan therapy because of mild symptoms and its
potential to enhance LPA blood flow and thereby left ventricular
volume load.
Create date
06/04/2010 16:33
Last modification date
20/08/2019 15:01
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