Percutaneous occlusion of a pulmonary aneurysm causing hemoptysis in a patient with pulmonary atresia and aortopulmonary collaterals (original) (raw)
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Internal medicine (Tokyo, Japan), 2017
The patient was a 19-year-old woman who was diagnosed with patent ductus arteriosus complicating Eisenmenger syndrome at a previous medical institution. She was referred to our hospital and arranged for lung transplantation. She developed hemoptysis after the introduction of i.v. epoprostenol, which was administered as a bridging treatment while the patient awaited lung transplantation. She continued to suffer from recurrent hemoptysis, even after switching from i.v. epoprostenol to i.v. treprostinil. Angiography of the systemic and pulmonary arteries revealed the vessel responsible for the recurrent hemoptysis and pulmonary artery embolization was successfully performed. It is essential to identify the culprit vessel and surgeons must not hesitate in performing embolization when patients develop lethal hemoptysis.
Unilateral pulmonary artery agenesis: An unusual cause of hemoptysis
Respiratory medicine case reports, 2023
Unilateral pulmonary artery agenesis (UPAA) is a rare malformation that can present as an isolated anomaly or may be associated with certain congenital cardiac anomalies, such as tetralogy of Fallot, atrial septal defect, coarctation of aorta, right aortic arch, truncus arteriosus and pulmonary atresia. Clinical presentation is nonspecific which makes the diagnosis elusive; chronic dyspnea, hemoptysis or recurrent infections are the most common manifestations. Patients may remain asymptomatic until adulthood. There is no definitive treatment for patients with UPAA. Acute respiratory distress syndrome (ARDS) is usually a bilateral disease, unilateral ARDS has been described after lung resection or trauma. We present a case of a 39 year-old woman who developed unilateral ARDS and was later diagnosed with isolated UPAA.
Young onset hemoptysis: A rare cause of pulmonary arterial aneurysm
Lung India, 2016
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Journal of cardiology, 2005
A 62-year-old woman was admitted to our hospital because of fever in August 2002. She had been treated under a diagnosis of Eisenmenger syndrome with ventricular septal defect since 1988. On admission, echocardiography and color Doppler echocardiography revealed a markedly enlarged pulmonary artery with a mobile flap, and dissection of the pulmonary artery. The origin of the fever could not be identified, and the fever subsided spontaneously without specific treatment. She had no chest pain, but fever might have been a sign of dissection in this patient. Longstanding pulmonary hypertension may cause dissection, which may lead to sudden death or pulmonary hemorrhage often seen in patients with Eisenmenger syndrome. Our patient was a rare survivor without serious bleeding complication.
Right pulmonary artery occlusion by an acute dissecting aneurysm of the ascending aorta
Journal of cardiothoracic surgery, 2006
We describe the case of a 76-year old female who presented with a Type A aortic dissection requiring repair with an interposition graft and aortic valve replacement. Post-operatively she had clinical features and computerised tomographic images suggestive of a pulmonary embolus and died 24 hours later. The extremely rare finding of intramural thrombus occluding the right pulmonary artery was seen at post mortem.
Heart & Lung: The Journal of Acute and Critical Care, 2013
The left-main coronary artery extrinsic compression due to enlarged pulmonary artery has been described in several case series. Ortner's syndrome is also a rare condition in some cardiovascular disorders. There have been no reports about these two rare conditions in the same patient. Hence, we report a very rare case of an Eisenmenger patient with severe pulmonary hypertension and dilated pulmonary artery which has compressed the left main coronary artery, severely narrowing it, and the left laryngeal recurrent nerve with subsequent Ortner's syndrome and brief literature review.
European Journal of Cardio-thoracic Surgery, 2003
Objectives: To validate the preliminary surgical results of 'integrated approach' to pulmonary atresia, ventricular septal defect (VSD), and multiple aortopulmonary collateral arteries by retrospective analysis of our center experience. Methods: Between 01/94 and 03/02, 37 patients aged 22 days to 13 years underwent surgery for pulmonary atresia, VSD, and multiple aortopulmonary collaterals. Case selection was based on preoperative calculation of total neopulmonary arterial index (TNPAI), pulmonary arterial index (PAI), and pulmonary arteries-to-collateral arteries lung segment perfusion ratio (S pa :S ca ). The decision for a possible VSD closure during one-stage procedures was based on an intraoperative pulmonary flow study. Twenty-five patients with a TNPAI equal to or greater than 150 mm 2 /m 2 underwent primary unifocalization, irrespective of PAI and S pa :S ca . Conversely, 12 patients with a TNPAI less than 150 mm 2 /m 2 and hypoplastic (PAI less than 100 mm 2 /m 2 ) dominant (S pa :S ca greater than 1) pulmonary arteries received a first-stage right ventricular outflow tract reconstruction, followed by unifocalization and repair (i.e. VSD closure) in nine cases. Results: Among 34 patients who received total unifocalization, the overall repairability rate was 85% (first instance repairs: n ¼ 27; delayed VSD closure: n ¼ 2; 95% confidence interval, CI: 73 -97%), with a survival rate at 7 years of 81%. Repaired survivors (n ¼ 26) are asymptomatic (n ¼ 22) or mildly symptomatic (n ¼ 4) at a follow-up interval of 43^28 months, with a 0.48^0.2 mean haemodynamic right ventricular/left ventricular pressure ratio, whereas palliated ones are waiting for either repair (n ¼ 3) or catheter study (n ¼ 2). Analysis of results has shown the following: (1) 100% (34/34 cases) feasibility of one-stage unifocalization in patients with a preoperative TNPAI equal to or greater than 150 mm 2 /m 2 , whereas combined repairability rate was 79% only (95% CI: 65-93%); (2) 100% (12/12 cases) fulfillment of criteria for second-stage repairability (acquired TNPAI greater than 150 mm 2 /m 2 ) in all patients treated with right ventricular outflow tract reconstruction; and (3) 93% (95% CI: 83-100%) overall accuracy of intraoperative flow study in predicting either postrepair mean pulmonary arterial pressure (VSD closed: n ¼ 23) or balanced pulmonary to systemic blood flow ratio (VSD left open: n ¼ 4). Conclusions: Increasing experience with 'integrated approach' to pulmonary atresia, VSD, and multiple aortopulmonaty collaterals has confirmed the preliminary results of our surgical series. The pulmonary flow study remains the most accurate intraoperative test for successful management of VSD during unifocalization procedures q
The Annals of Thoracic Surgery, 1991
Fifty-eight consecutive patients with pulmonary atresia, ventricular septal defect, hypoplastic pulmonary arteries with arborization defects, and major aortopulmonary collaterals were entered into a program for staged surgical repair between January 1979 and July 1989. Prerepair preparatory procedures were designed to (1) encourage native pulmonary artery growth by increasing blood flow and (2) unifocalize pulmonary blood supply by transplanting or ligating major collaterals. A total of 121 staging procedures were performed with an overall mortality of 10.3%. One hundred thirty-four major collaterals atients with pulmonary atresia and ventricular septal P defect (VSD) are not suitable for one-stage repair when the pulmonary arteries are hypoplastic and have severe arborization defects and when sizeable portions of the lungs are supplied by major systemic to pulmonary collateral arteries (MAPCAs) [l]. These patients have long been managed with palliative shunt procedures [2] or palliative gusset repair [3] of the right ventricular outflow tract. Experience with systemic to pulmonary shunts in tetralogy of Fallot has revealed that hypoplastic pulmonary arteries can be induced to grow by increasing blood flow in them [4, 51. Hemodynamic repair of pulmonary For editorial comment, see page 8.