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(Circulation. 2000;102:III-142.)
© 2000 American Heart Association, Inc.

Surgery for Congenital Heart Disease

Severe Airflow Limitation After the Unifocalization Procedure

Clinical and Morphological Correlates

Ingram Schulze-Neick, MD; S. Yen Ho, PhD; Andrew Bush, MD; Mark Rosenthal, MD; Rodney C. Franklin, MD; Andrew N. Redington, MD; Daniel J. Penny, MD

From the Great Ormond Street Hospital for Children NHS Trust and the Royal Brompton and Harefield NHS Trust (S.Y.H., A.B., M.R., R.C.F.), London, England.

Correspondence to Dr D.J. Penny, Cardiothoracic Unit, Great Ormond Street Hospital for Children NHS Trust, London, UK WC1. E-mail dan.penny{at}gosh-tr.nthames.nhs.uk

Background—While unifocalization techniques have improved the treatment options in patients with pulmonary atresia, ventricular septal defect (PA-VSD), and major aortopulmonary collaterals (MAPCAs), severe airflow limitation contributes to significant early postoperative morbidity and mortality. Although this has been attributed to bronchospasm, characteristically it is refractory to bronchodilators, suggesting that other mechanisms may play a role.

Methods and Results—The clinical course and preoperative angiograms of patients who underwent unifocalization were reviewed. Patients who developed airflow limitation early after surgery underwent fiberoptic bronchoscopy. In addition, the anatomy of the MAPCAs was examined in 14 heart-lung blocks from patients with PA-VSD. Twenty-two procedures were performed in 16 children. Three developed marked airflow limitation early after surgery, necessitating prolonged high-pressure ventilation. Bronchoscopy demonstrated tracheobronchial epithelial necrosis in 2 and signs of tracheobronchial ischemia in the third. Two were successfully extubated after 15 and 16 days, but the third died after 57 days of ventilatory support. Review of the preoperative angiograms demonstrated an extensive peribronchial arterial supply arising from a MAPCA in 1 of the patients who developed severe airway necrosis after unifocalization. This was also obvious in a second patient, but the MAPCA was not included in the unifocalization. In 7 autopsy specimens, MAPCAs contributed to a peribronchial or peritracheal vascular network. Dissection of the distribution of these branches in 2 specimens revealed extensive intrapulmonary peribronchial anastomoses.

Conclusions—Airflow limitation early after unifocalization is related to airway ischemia resulting from interruption of the tracheobronchial blood supply during mobilization of MAPCAs.

Key Words: heart defects, congenital • surgery • ventilation • complications

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