Division Of Patent Ductus Arteriosus Research Articles

Staged surgical repair for infants with interrupted aortic arch

BackgroundInterrupted aortic arch (IAA) is a rare congenital cardiac anomaly, which necessitates surgical treatment. There are several surgical strategies for corrective repair of IAA, such as one-stage repair, rapid two-stage repair and two-stage repair. Here, we reported our surgical result of staged-repair policy for the patients with IAA. MethodFrom November 2003 to July 2015, there were 14 patients (8 boys, 6 girls) with IAA treated by us. Except one teenager patient, we routinely used intravenous infusion of prostaglandin E1 for all the infant patients (n = 13) to keep adequate end organ perfusion before the first surgical intervention. Surgical repair was performed after the perfusion of end organs recovered. ResultTwo patients (1 teenager and 1 infant with one-stage surgery) were excluded from this study. At the time of the first surgery, we did the first-stage surgery with anastomosis in between aortic arch and descending aorta, division of patent ductus arteriosus and banding of pulmonary trunk through left thoracotomy. The overall surgical survival rate of the first surgery was 100% (12/12). At the time of the second surgery, corrective repair was done under cardiopulmonary bypass through median sternotomy. The surgical survival rate of the corrective surgery was also 100%. There is no late death during follow-up for 9 years (range 4.2–15.0 years). ConclusionOut of several surgical strategies for the infants with IAA, staged repair still could be a treatment option to achieve satisfied surgical result.

Repair of congenital tracheal stenosis with a free tracheal autograft

Objectives: Evaluate the results of a technique for repair of congenital tracheal stenosis by use of a free tracheal autograft. Methods: Between January 1996 and July 1997, six infants with congenital tracheal stenosis resulting from complete tracheal rings underwent repair with a free tracheal autograft. Mean age at the time of repair was 4.9 months; mean weight was 5.4 kg. The approach was through a median sternotomy with cardiopulmonary bypass for respiratory support. The trachea was incised anteriorly through the area of stenosis, the midportion of the stenotic trachea was excised, and an end-to-end anastomosis was carried out posteriorly. The excised tracheal segment (1.3 to 2.2 cm long) was used as a free autograft to patch the lower trachea anteriorly. In four infants the autograft was augmented in the upper trachea with pericardium; in two patients with a shorter length of stenosis, the autograft completed the repair. Simultaneous pulmonary artery sling repair (4), ligation and division of patent ductus arteriosus (3), cricoid split (2), atrial and ventricular septal defect repair (1), and complete atrioventricular canal repair (1) were performed at the time of tracheal repair. Results: The infants were extubated and discharged at a mean of 13 and 23 days postoperatively, respectively. One infant had recurrent tracheal stenosis related to the pericardial patch and required a tracheal stent and tracheostomy 4 months postoperatively. Our mean follow-up is 11 months. Bronchoscopic findings currently show widely patent tracheal lumina in all infants. Conclusions: The technique of free tracheal autograft with and without pericardial augmentation was successful in opening the airway of six infants with congenital tracheal stenosis and is currently our procedure of choice for children with this diagnosis. (J Thorac Cardiovasc Surg 1998;115:869-74)

False aneurysm as a late complication of division of a patent ductus arteriosus

A 58-year-old male patient who had a huge false aneurysm as a late sequela of division of patent ductus arteriosus was surgically managed with success. It is noteworthy that 24 years had elapsed from the initial operation until recognition of the aneurysm. The pathogenesis and method of the surgical treatment are discussed.

The pharmacological treatment of patent ductus arteriosus. A review of the evidence.

Modern heart surgery began with operative intervention for patent ductus arteriosus in 1938. Half a century later, ligation and division of patent ductus arteriosus in an infant or child remains a simple and safe surgical procedure for a lesion identified relatively easily. In the intervening years, paediatric cardiologists and surgeons have also directed their attention to the management of more complex congenital cardiac defects. Recently, however, there has been a significant reappraisal and re-emphasis of the role of patent ductus arteriosus in the context of neonatal cardiopulmonary disease. Interest has focused on: (a) surgical and pharmacological management of the premature infant with a large ductal left-to-right shunt in the context of respiratory distress syndrome; (b) preservation of patency in ductal-dependent congenital heart disease; and (c) ductal right-to-left shunting in persistence of the fetal circulation (PFC) syndrome or other diseases associated with increased pulmonary vascular resistance. This review examines the above conditions and reviews the progress and current status of drug therapy in the treatment of these disorders. Closure of the ductus arteriosus with cyclo-oxygenase inhibition as well as re-opening and maintaining patency of the ductus arteriosus with prostaglandin therapy is discussed.

Division of patent ductus arteriosus by "isthmus taping method".

"Isthmus taping method" as the safe and simple technique for division of patent ductus arteriosus (PDA), along with surgical and follow-up results were reported. 175 patients with PDA and without other cardiac anomalies were operated by this technique. Most of the patients were operated by junior surgeons as a first step in cardiac surgery. The left chest was entered through posterolateral thoracotomy in the third or fourth intercostal space. Tapes were placed around the isthmus of aorta and PDA. Intercostal arteries were not divided. PDA was divided in-between Potts' clamps. Pulmonary and aortic stumps of the PDA were closed with two rows of continuous over and over suture. Of the 175, one patient (0.6%) with pulmonary hypertension died of postoperative respiratory failure. No surgical hazards of bleeding were noted. No deaths were noted among 131 patients without pulmonary hypertension. Follow-up results in 174 patients up to 14 years were excellent.

Ostium secundum atrial septal defects and congestive heart failure in infancy

Foramen secundum defects of the interatrial septum with large left to right shunts may cause congestive heart failure during infancy. In three infants with this lesion, varying in age from 5 days to 2 years, intractable congestive heart failure developed. Case 1 presented with signs of congestive heart failure in the newborn nursery. She failed to respond to the usual anticongestive measures. At 6 weeks of age her defect was reduced in size by the external closure technic of Sondergaard. She had an excellent postoperative course. Case 2 presented in severe congestive heart failure at 3 months of age. Clinical improvement followed ligation and division of a large patent ductus arteriosus. Signs of cardiac decompensation reappeared at 6 months. Closure of a secundum atrial septal defect on cardiopulmonary bypass was successful. The oldest child, a 2 year old female, presented with severe congestive heart failure of unknown duration. An attempt was made to close her atrial septal defect with cardiopulmonary bypass. Her death following surgery was apparently due to almost complete pneumonic consolidation of her lungs. Each of these female infants had distinctive physical findings which led to the correct clinical diagnosis of their lesion. In Case 2 the physical findings appeared after ligation and division of the patent ductus arteriosus. These physical signs were: a right ventricular systolic thrust along the lower left sternal margin, a harsh systolic ejection murmur along the left sternal border associated with a palpable systolic thrill, and a wide and fixed split of the second heart sound at the cardiac base. In addition to the physical findings, the electrocardiogram showed right atrial enlargement and right ventricular hypertrophy. Chest roentgenograms demonstrated moderate to marked heart enlargement with increased pulmonary blood floW. Our experience with these infants demonstrates again that foramen secundum interatrial septal defects may be lethal lesions and may be responsible for considerable morb dity during infancy. The gratifying postoperative course following partial closure of the defect of the atrial septum by the Sondergaard technic in the small infant suggests that this technic should be evaluated further as a palliative procedure for small infants in congestive heart failure caused by this lesion.

The technique of surgical division of patent ductus arteriosus: Wangensteen, O. H., Varco, R. L., and Baronofsky, I. D.: Surg., Gynec. & Obst. 88:62 (Jan.), 1949

The technique of surgical division of patent ductus arteriosus: Wangensteen, O. H., Varco, R. L., and Baronofsky, I. D.: Surg., Gynec. & Obst. 88:62 (Jan.), 1949

Circulatory changes produced by clamping of the thoracic aorta.

URGICAL excision of the anomalous segment of aorta for treatment of eongenital coarctation of that vessel was reported in 1945 by Crafoord and Nylin’ and Gross and Hufnagel.’ Clamps were applied to the aorta above and below the usual site of coarctation at the liganzentunz arterioszcnz. The proximal clamp was applied just distal to the left subelavian artery so that circulation t#o the head and upper extremities was unimpaired. Blood flow dkM to the clamps was maintained through collateral channels around the obstmetion. After the constricted segment of aorta had been excised, continuity of the vessel was re-established by end-to-end anastomosis. In the first human being operated upon by Gross, immediately after the clamps were released, the heart went into uncontrollable dilatation and the patient died2p ‘3 4 Gross thought that the failure was caused by inadequate return of blood to the heart after the clamps were released. In his subsequent operations the clamps were released slowly over a period of minutes with the patient in the Trendelenburg positiqn. The rate of blood infusion was increased during the period of unclamping. After these precautions were adopted, no further deaths were reIjorted. Concerning the cause of heart failure; Gross sa.id,4 “From some of our experimental work, and from a disastrous outcome in one ease, it is evident that a quick Ternoval of the last aortic clamp may impose a momentary but serious burden on the cardio-vascnlar apparatus. The sudden opening np of an enormous vascular bed in the lower part of the body makes great demands upon the heart. The cause of death in the first patient has been loosely described as ‘cardiac collapse’ since the exact mechanism of failure is not known. Presumably, it was a form of ‘shock’ because blood flowed rapidly into Dhe depleted system in the lower two-thirds of the body, pooled there; and did not return quickly enough to supply the heart with a circulating medium.” Crafoord had not observed such cardiac failure despite experience with the aortic occlusion maneuver both during excision of coarctation and during division of patent ductus arteriosus.5 In view of the added strain imposed upon the heart by such obstruction, and the abnormal conditions which must prevail immediately after release of the clamps, the following .esperiments were carried out in an effort to determine whether the failure could be explained by existing concepts or whether factors hitherto undescribed played a part,.