The St. Jude Medical cardiac valve in infants and children: role of anticoagulant therapy.

The experience at the University of Colorado with the St. Jude Medical cardiac valve was reviewed to determine the feasibility of placing this prosthesis in children and the role of anticoagulation. A St. Jude Medical cardiac valve was placed in 33 patients ranging in age from 2.5 months to 17 years. Seven patients were less than 1 year of age. Nineteen valves were placed in the aortic position in patients aged 5 months to 17 years (mean 9.5 years). Five patients had valve replacement only, 13 had concomitant aortoventriculoplasty and 1 a Manouguian procedure. Indications for anulus enlarging procedures were recurrent subaortic stenosis or inability to place an adult-sized valve in the native aortic anulus, or both. There were no early or late deaths. Fourteen valves were placed in the mitral position. They were anular positioned in 6 patients aged 6 months to 16 years and supraanular positioned in 8 patients aged 2.5 months to 2 years. There were no deaths with the anular positioned replacements and seven deaths (two early and five late) with the supraanular positioned replacements. Four of the five late deaths were associated with marked pre- and postoperative left ventricular dysfunction. The follow-up time was 784 patient-months in 31 long-term survivors. Anticoagulation was achieved with warfarin, usually in combination with sulfinpyrazone, dipyridamole or aspirin. There were four episodes of thromboembolism, three occurring in patients with suboptimal anticoagulation, and one in a patient lost to follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

The changing spectrum of pulmonary operations in infants and children.

During the 37 year period between 1943 and 1980, 68 pediatric patients underwent 86 major pulmonary resections during 73 separate operations. The surgical procedures included lobectomy (55), segmentectomy (25), pneumonectomy (three), and cyst excision (three). The 73 operations were performed for nontuberculous infection, congenital malformation, tuberculosis, tumor, obstructive lung disease, cardiac-related problems, immunologic disease, and trauma in decreasing order of frequency. The operative mortality was 4.4%; the disease-relate late mortality was 6.2%, due to either chronic respiratory failure or metastatic disease. Complications occurred in 21.9% of the operations. Only one death occurred during the last two decades, but the morbidity rate remained constant through all decades. Analysis by decade showed a striking change in the spectrum of pediatric pulmonary operations over the 37 year study period. Three major trends were identified: (1) Bronchiectasis and tuberculosis, once the major indications for pulmonary resection, have, from a surgical standpoint, virtually disappeared. (2) Congenital pulmonary anomalies now account for the majority of major pediatric pulmonary resections. As a consequence, the patient age at operation has steadily decreased, and pulmonary resections in infants (under 1 year of age) make up almost half of the surgical resections currently being done. (3) Despite the marked decline in the number of operations performed for infectious pulmonary disease, the total number of pulmonary operations in the pediatric age group has not decreased.

Pulmonary allograft conduit repair of tetralogy of Fallot. An alternative to transannular patch repair.

Cryopreserved allograft valves and valved conduits have been used in 122 patients during the past 3 years for surgical repair of congenital heart disease. In 55 of these patients, the right ventricular outflow tract was reconstructed with a pulmonary allograft conduit. Although most children requiring a conduit had complex lesions, 12 patients with tetralogy of Fallot without pulmonary atresia or absent valve syndrome have been treated in this manner since April 1985. Patients were selected for conduit therapy because of congenital or iatrogenic pulmonary artery problems (nine patients had 12 prior shunts) or increased pulmonary vascular resistance. Ages ranged from 7 months to 6 years (mean 3.1 years) and weights from 7.4 to 18.5 kg (mean 12.2 kg). Pulmonary artery conduit size ranged from 16 to 24 mm internal diameter (mean 22 mm). Distal pulmonary artery reconstruction beyond the bifurcation was required in nine patients and the proximal connection was completed with a hood-shaped patch. One operative death (8.3%) occurred at 20 days as a result of severe right ventricular dysfunction. Left pulmonary artery thrombosis was discovered postmortem. Eleven survivors observed for 3 to 37 months (mean 17 months) are without cardiac symptoms. A chronologically overlapping group of tetralogy of Fallot repairs accomplished with a transannular patch was also reviewed. Twenty-five patients aged 2 months to 4 years (mean 1.7 years) and weighing 3.6 to 14.8 kg (mean 9.2 kg) underwent this procedure from April 1983 to January 1987 (seven patients had one prior shunt each). The mortality rate in this group was 28% (six operative deaths and one late death). Of 18 survivors observed from 20 to 60 months (mean 41.4 months), five (28%) have required pulmonary artery conduit reconstruction for chronic right ventricular failure. Postrepair right ventricular/left ventricular pressure ratios were available in 19 patients, including five of seven who died and three of five who required reoperation. The ratios averaged 0.54, which indicates adequate relief of obstruction. The operative mortality rate from a number of series for transannular patch repair of tetralogy of Fallot averages 16%, ranging from 3% to 63%. However, when distal pulmonary artery problems are added as a risk factor this rate rises to 21%, and valved conduit insertion increases the mortality rate (Kirklin and Barratt-Boyes, 1986). Although not clearly superior, pulmonary artery conduit repair of tetralogy of Fallot achieves results comparable with those of transannular patch repair and is recommended as an alternative, particularly when distal pulmonary artery anatomy is abnormal or vascular resistance is elevated.

Experience with operations for hypoplastic left heart syndrome.

Aortic atresia is a form of congenital cardiac disease complicated by associated severe hypoplasia of the ascending aorta and various degrees of mitral valve and left ventricular hypoplasia. Occasionally, neonates with severe aortic stenosis have associated severe hypoplasia of the ascending aorta and left ventricle. These two defects constitute the most prevalent forms of so-called hypoplastic left heart syndrome. At present, this lesion is universally fatal with no established surgical management. This report describes our experience with the evolution and evaluation of staged surgical management of infants with hypoplastic left heart syndrome.

Extended aortic root replacement with aortic allografts.

Complex left ventricular outflow tract obstruction after operation for subaortic stenosis or with hypoplastic aortic anulus remains a challenge for pediatric cardiac surgeons. We have recently applied a new technique of extended aortic root replacement using a cryopreserved aortic allograft to treat two patients who had previously been operated on for subaortic stenosis and a third who had aortic stenosis with a hypoplastic aortic anulus. This new procedure combines the concept of aortoventriculoplasty with aortic root replacement and coronary artery reimplantation. The valved aortic homograft is used in place of an aortic valve prosthesis and the attached anterior mitral leaflet augments the interventricular septum to relieve the subvalvular left ventricular outflow tract obstruction. The coronary ostia are then reimplanted into the allograft and an anastomosis between the distal graft and the ascending aorta is completed. Allograft aortic tissue is then used to patch the right ventricular outflow tract. One patient had aortic stenosis with annular hypoplasia and did well after extended root replacement. Two patients had previous operations for subaortic stenosis before undergoing extended aortic root replacement. One required mediastinal exploration and drainage at 2 weeks for Serratia marcescens mediastinitis and bacteremia, but uncomplicated recovery followed. The other patient had complete heart block for 2 days, but normal sinus rhythm resumed and convalescence was benign. This modified technique with the aortic allograft was very helpful in treating these difficult problems, and the lack of mortality, limited morbidity, and good functional results are encouraging.

Aortoventriculoplasty in children.

Aortoventriculoplasty was performed in 16 children between July, 1980, and July, 1984. Indications for the procedure were 1) aortic stenosis or insufficiency, or both, necessitating replacement of an aortic valve whose anulus would not accept a 19 mm diameter valve, (2) replacement of a small valve prosthesis, or (3) recurrent tunnel subaortic stenosis. Patients were 5 months to 17 years old at operation, 14 had previous repairs, and four had prior aortic valve replacement. There were 13 long-term survivors followed up for 14 to 38 months; 12 are asymptomatic with normal exercise tolerance. Three had residual ventricular septal defects, two requiring repair. All patients were given warfarin with or without antiplatelet agents. There have been no thromboembolic episodes and no hemorrhagic complications. Aortoventriculoplasty is well tolerated in children and appears to be a viable surgical option in the management of young patients with a hypoplastic left ventricular outflow tract.

Conduit reconstruction of the right ventricular outflow tract. Lessons learned in a twelve-year experience.

From September 1979 to July 1991, a total of 163 patients have undergone valved conduit reconstruction of the right ventricular outflow tract when a right ventricle-pulmonary artery connection was absent or right ventricular outflow tract enlargement was required. From September 1979 through October 1984, 24 porcine valved conduits were implanted with an operative mortality of 38% (9/24). There were no early failures, but by 9 years after the operation 9 of 15 survivors (60%) had severe conduit obstruction, which resulted in death in 2 patients and reoperation in 6. From May 1985 to June 1991, 24 patients received cryopreserved aortic allografts to correct congenital anomalies. Operative mortality was 25% (6/24) and, again, early conduit function was good. There were 4 (22%) late deaths that were not related to the aortic allograft. At a mean follow-up of 3.4 years, 11 of the 13 survivors (85%) had allograft calcification and 8 of the 13 (62%) had mild to moderate conduit stenosis or regurgitation, or both; two of them required conduit replacement. Distal anastomotic problems that might have been avoided with bifurcated pulmonary allografts were apparent in 4 (36%) patients. Cryopreserved pulmonary allografts were placed in 115 patients between April 1985 and January 1991, with 18 (16%) operative deaths. Late deaths that were not allograft related occurred in 7 of 97 surviving patients (7%). Six patients (6%) underwent reoperation, 2 because of primary pulmonary allograft failure. The 84 remaining patients are free of symptoms with little or no allograft calcification or echocardiographic evidence of significant conduit stenosis or regurgitation. Experience with porcine valved conduits and aortic and pulmonary allografts suggests that pulmonary allografts are the conduit of choice for right ventricular outflow tract reconstruction.

Lung transplantation with cardiopulmonary bypass exaggerates pulmonary vasomotor dysfunction in the transplanted lung.

Pulmonary vascular resistance is significantly increased in the transplanted lung. If cardiopulmonary bypass is required, the transplanted lung is reperfused with activated blood elements, which might exacerbate the reperfusion injury. The purpose of this study was to examine the influence of cardiopulmonary bypass on the following mechanisms of pulmonary vasomotor control in a dog model of autologous lung transplantation: (1) endothelium-dependent cyclic guanosine monophosphate-mediated relaxation (response to acetylcholine), (2) endothelium-independent cyclic guanosine monophosphate-mediated relaxation (response to nitroprusside), and (3) beta-adrenergic cyclic adenosine monophosphate-mediated relaxation (response to isoproterenol). Autologous right lung transplants were performed with (n = 4 dogs) and without (n = 5 dogs) bypass. Lungs were stored in cold saline solution (4 degrees C, 3 hours) before reimplantation. Pulmonary vasomotor control mechanisms were studied in isolated pulmonary arterial rings immediately after harvest and 1 hour after reimplantation. Ten rings were studied in each group at each time. Statistical analysis was by analysis of variance. Without bypass, endothelium-dependent cyclic guanosine monophosphate-mediated relaxation and beta-adrenergic cyclic adenosine monophosphate-mediated relaxation were significantly impaired, although endothelium-independent cyclic guanosine monophosphate-mediated relaxation was not. Use of bypass produced significantly greater impairment of both endothelium-dependent cyclic guanosine monophosphate-mediated relaxation and beta-adrenergic cyclic adenosine monophosphate-mediated relaxation. In addition, use of bypass produced significant dysfunction of endothelium-independent cyclic guanosine monophosphate-mediated relaxation as well. We conclude that using cardiopulmonary bypass to perform lung transplantation greatly exaggerates pulmonary vasomotor dysfunction in the transplanted lung. This dysfunction may contribute to significantly higher pulmonary vascular resistance in the transplanted lung if cardiopulmonary bypass is used.

Degeneration of aortic valve allografts in young recipients.

Aortic allograft fibrocalcification and valvular insufficiency have been observed in patients less than 3 years of age at initial replacement of the left ventricular outflow tract. From June 1985 through May 1992, 47 children have undergone aortic root replacement with cryopreserved aortic valve allografts. Thirty-three children were 3 years of age or older and 14 were less than 3 years of age at operation. In the older patient group, there were three (9%) hospital deaths and one child underwent cardiac transplantation 30 hours after aortic root replacement because of left ventricular failure. Clinical follow-up of the 29 surviving older children is from 4 months to 6.6 years (mean 3.0 years). One patient was lost to follow-up. Two children (7%) have required reoperation, but primary allograft degeneration was not observed. In the younger patient group, there were three (21%) hospital deaths. Follow-up ranged from 2.5 months to 4.7 years (mean 2.3 years). Among 11 operative survivors, one late death resulted from a pulmonary embolus. Seven of 10 (70%) remaining allograft recipients had progressive allograft calcification or insufficiency. Six of them have required reoperation to explant the allograft, and one child is currently receiving cyclosporine therapy with the original valve allograft. The cause of allograft failure is possibly immunologic. The prevalence of early aortic valve allograft degeneration has prompted the consideration of nonviable allografts or xenografts, pulmonary autografts, or minimal immunosuppression as alternatives when left ventricular outflow tract reconstruction is necessary in children less than 3 years of age.

Cardiac 5'-nucleotidase activity increases with age and inversely relates to recovery from ischemia.

The metabolic basis for the enhanced tolerance of immature hearts to ischemia remains to be elucidated. Loss of high-energy phosphate nucleotides occurs during ischemia/reperfusion in mature (adult) hearts through the breakdown of adenosine triphosphate, diphosphate, and monophosphate (nondiffusible) to adenosine (freely diffusible). However, previous work has shown that after ischemia nondiffusible nucleotides are better retained by immature (neonatal) hearts than by mature hearts. The enzyme responsible for the conversion of adenosine monophosphate to adenosine is 5'-nucleotidase. We therefore hypothesized lower activity of this enzyme in neonatal than in adult myocardium. The purposes of this study were (1) to document 5'-nucleotidase activities in neonatal and adult rabbit myocardium and (2) to correlate differences of 5'-nucleotidase activity with functional recovery from ischemia. Neonatal (5- to 10-day-old) and adult (4- to 6-month-old) rabbit hearts were isolated and perfused (retrograde Langendorff). A left ventricular balloon measured functional parameters. Hearts were subjected to 20 minutes of global 37 degrees C ischemia and 10 minutes of reperfusion followed by freeze clamping. Tissue homogenates were assayed for 5'-nucleotidase by the linked formation of nicotinamide-adenine dinucleotide at 340 nm (Arkesteijn method). Postischemic recovery of developed pressure was 86% +/- 3% in neonates (n = 5) versus 38% +/- 3% in adults (n = 8) (mean +/- standard deviation) (p less than 0.01). 5'-Nucleotidase activity was 4400 +/- 1208 nmol/min/gm in neonates (n = 5) versus 13,938 +/- 830 nmol/min/gm in adults (n = 8) (mean +/- standard deviation) (p less than 0.01). We conclude that (1) 5'-nucleotidase activity is 68% lower in neonatal than in adult myocardium and (2) functional recovery after ischemia inversely relates to 5'-nucleotidase activity.

Cold ischemia and reperfusion each produce pulmonary vasomotor dysfunction in the transplanted lung.

Pulmonary vascular resistance is significantly increased in the transplanted lung. We hypothesized that the ischemic or reperfusion injuries incurred by the transplanted lung may produce pulmonary vasomotor dysfunction, which in turn may produce increased pulmonary vascular resistance. In a dog model of autologous lung transplantation, the purpose of this study was to examine the following mechanisms of pulmonary vasomotor control and to relate each of them to cold ischemia and to reperfusion: (1) endothelium-dependent cyclic guanosine monophosphate-mediated vasorelaxation (response to acetylcholine 10(-6) mol/L), (2) endothelium-independent cyclic guanosine monophosphate-mediated vasorelaxation (response to sodium nitroprusside 10(-6) mol/L), and beta-adrenergic cyclic adenosine monophosphate-mediated vasorelaxation (response to isoproterenol 10(-6) mol/L). Autologous right lung transplantation was performed in five dogs. At each of three times, two third-order pulmonary arteries were dissected from each transplanted lung and studied: control (immediately after harvest), cold ischemia (3 hours in 4 degrees C saline solution), and cold ischemia plus reperfusion (1 hour after lung reimplantation). The vasorelaxing effects of acetylcholine, sodium nitroprusside, and isoproterenol were studied in isolated pulmonary arterial rings, suspended on fine wire tensiometers in individual organ chambers. Statistical analysis was by analysis of variance. Results demonstrated significant dysfunction of beta-adrenergic cyclic adenosine monophosphate-mediated relaxation after cold ischemia alone, and this dysfunction was exacerbated by reperfusion. Endothelium-dependent cyclic guanosine monophosphate-mediated relaxation was not impaired by cold ischemia alone but was significantly impaired by reperfusion. Endothelium-independent cyclic guanosine monophosphate-mediated relaxation was not impaired by cold ischemia or reperfusion. We conclude that cold ischemia and reperfusion each produce different patterns of pulmonary vasomotor dysfunction. Cumulatively, such dysfunction may contribute to increased pulmonary vascular resistance in the transplanted lung.

Paralyzed left vocal cord associated with ligation of patent ductus arteriosus.

We reviewed the records of 167 neonates and older children undergoing ligation of a patent ductus arteriosus to determine the prevalence of recurrent laryngeal nerve injury and identify risk factors that might increase the likelihood of injury. Paralysis or paresis of the left vocal cord was identified by fiberoptic laryngoscopy in seven patients. All seven weighted less than 1500 gm at the time of operation and the ductus had been ligated with a metal clip. All had persistent symptoms when observed for 5 to 19 months. Injury to the left recurrent laryngeal nerve occurs infrequently but may have long-term consequences.

Infant heart transplantation: improved intermediate results.

OBJECTIVES: Our objectives were to (1) review our experience with heart transplants in infants (age < 6 months), (2) delineate risk factors for 30-day mortality, and (3) compare outcomes between our early and recent experience. METHODS: Records of all infants listed for transplantation in our center before September 1996 were analyzed. Early and recent comparisons were made between chronologic halves of the accrual period. Univariate analysis was used to analyze potential risk factors for 30-day mortality (categorical variables, Fisher's exact test; continuous variables, nonparametric Wilcoxon rank-sum test). Multivariable analysis included univariate variables with p values < or = 0.10. Actuarial survivals were estimated (Kaplan-Meier) and compared by the log-rank test. RESULTS: Fifty-one of the 60 infants listed for transplantation were operated on (waiting list mortality 15%). Thirty-day mortality was 18% overall, 30% in the first 3 years and 10% in the last 3 years (p = 0.07). Sepsis was the commonest cause of early death (4/9). Univariate analysis suggested four potential risk factors for early death: preoperative mechanical ventilation (p = 0.01), prior sternotomy (p = 0.002), preoperative inotropic drugs (p = 0.08), and warm ischemia time (p = 0.08). Multivariable analysis indicated that prior sternotomy (p = 0.01) was an independent risk factor for 30-day mortality. Actuarial survivals were 80%, 78%, and 70% at 1, 2, and 3 years, and these figures improved between early and recent groups (p = 0.05). Late deaths were most commonly due to acute rejection (3/5). CONCLUSIONS: Results of heart transplantation in infancy improve with experience. Prior sternotomy increases initial risk. Intermediate-term survival for infants with end-stage heart disease is excellent.

Secondary pulmonary hypertension does not adversely affect outcome after single lung transplantation.

OBJECTIVE: Primary and secondary pulmonary hypertension have been associated with poor outcomes after single lung transplantation. Some groups advocate double lung transplantation and the routine use of cardiopulmonary bypass during transplantation in this population. However, the optimal procedure for these patients remains controversial. The goal of our study was to determine the safety of single lung transplantation without cardiopulmonary bypass in patients with secondary pulmonary hypertension. METHODS: We retrospectively reviewed 76 consecutive patients with pulmonary parenchymal disease who underwent single lung transplantation from 1992 to 1998. Recipients were stratified according to preoperative mean pulmonary artery pressure. Secondary pulmonary hypertension was defined as parenchymal lung disease with a preoperative mean pulmonary artery pressure of 30 mm Hg or more. Patients with primary pulmonary hypertension or Eisenmenger's syndrome were excluded from analysis. RESULTS: Eighteen of 76 patients had secondary pulmonary hypertension. No patient with secondary pulmonary hypertension required cardiopulmonary bypass, whereas 1 patient without pulmonary hypertension required bypass. After the operation, no significant differences were seen in lung injury as measured by chest radiograph score and PaO(2)/FIO(2) ratio, the requirement for inhaled nitric oxide, the length of mechanical ventilation, the intensive care unit or hospital length of stay, and 30-day survival. There were no differences in the forced expiratory volume in 1 second or 6-minute walk at 1 year, or the incidence of rejection, infection, or bronchiolitis obliterans syndrome greater than grade 2. Survival at 1, 2, and 4 years after transplantation was 86%, 79%, and 65%, respectively, in the low pulmonary artery pressure group and 81%, 81%, and 61%, respectively, in the group with secondary pulmonary hypertension (P >.2). CONCLUSION: We found that patients with pulmonary parenchymal disease and concomitant secondary pulmonary hypertension had successful outcomes as measured by early and late allograft function and appear to have acceptable long-term survival after single lung transplantation. Our results do not support the routine use of cardiopulmonary bypass or double lung transplantation for patients with this disorder.

Utility of extracorporeal membrane oxygenation for early graft failure following heart transplantation in infancy.

BACKGROUND: Extracorporeal membrane oxygenation (ECMO) is widely used for postcardiotomy cardiogenic shock in children. However, the efficacy of ECMO for early post-heart transplant graft failure in infants has not been reported. Our aims were to determine: (1) the utility of ECMO in infants with severe donor-heart dysfunction, (2) predictors for requiring ECMO, and (3) the long-term outcome of surviving ECMO patients. METHODS: All infants (age < 6 months at listing) undergoing heart transplantation were reviewed. Diagnostic categories were hypoplastic left heart syndrome (HLHS) and non-HLHS (complex congenital heart disease and cardiomyopathies). Continuous and categorical comparisons were by Wilcoxon's rank sum test and Fisher's exact test respectively. RESULTS: 14 (12 HLHS, 2 non-HLHS) of 63 (46 HLHS, 17 non-HLHS) infants were placed on ECMO. Ten patients (71%) were successfully weaned from ECMO and 8 (57%) were discharged alive. All ECMO hospital survivors remain alive (mean follow-up 36.2 +/- 21.4 months, range 13.1-77.6 months). Mean duration of ECMO support was 68 hours in weaned patients vs 144 hours (p = 0.19) in nonweaned patients, and 64 hours in survivors vs 123 hours (p = 0.35) in nonsurvivors. ECMO deaths were due to sepsis (n = 3), intractable pulmonary hypertension (n = 2), and intracranial bleed (n = 1). Neurologic deficits occurred in 2 survivors. Median ICU and hospital stays for ECMO survivors were 29 and 33 days vs 7 (p = 0.0003) and 9 (p = 0.0004) days for non-ECMO patients. Age listed, age transplanted, wait time, body weight, donor/recipient weight ratio, total ischemia time, and diagnosis did not predict the need for ECMO. CONCLUSIONS: (1) ECMO is useful for post-heart transplant circulatory support in infants with early graft failure. (2) All survivors were weaned in fewer than 4 days. (3) Three-year survival of ECMO hospital survivors has been high, but neurologic complications are prevalent.

Indications and contraindications for heart transplantation in infancy.

Heart transplantation uniquely offers infants with irreversible myopathies and complex congenital heart disease (CCHD) the potential for survival. Heart transplantation in the first year of life has an actuarial 1-year survival rate of 85%. Controlling for the variables that lead to perioperative death can improve 1-year survival rates to 95%. Mortality is also accrued before transplantation, with 15% to 20% of infants dying before a donor organ is available. Because of this cumulative mortality, an algorithm was developed to maximize pre- and posttransplantation survival and thus increase the likelihood that the limited donor supply would have the greatest impact. The risk factors considered in the algorithm include: (1) hemodynamic stability, (2) central venous access/prostaglandin requirements, (3) need for ventilator support, (4) pulmonary blood flow dependent on a critically restricted atrial septal defect, (5) risk for pulmonary hypertension, (6) anomalous pulmonary venous return, and (7) history of sepsis. Overall, patient survival would be maximized by only using transplantation for patients with CCHD who have moderate or less risk of pre- or posttransplantation death (< 20%). Donor organ utilization could be maximized by reserving transplantation for patients without options (myopathies) and for patients with CCHD who have a low predicted risk of death (< 10%). Because the risks of death at transplantation or in the first year after transplantation are low and relatively fixed, changes in risks of palliative surgery or donor availability can be easily used to adjust the decision algorithm.

A dual approach to tracheobronchial foreign bodies in children.

From 1974 to 1980, 57 consecutive cases of children with tracheobronchial foreign bodies were treated by a new protocol in which peripherally located foreign bodies were treated nonoperatively and centrally located foreign bodies were removed bronchoscopically. Bronchoscopic removal was ultimately successful in all of the 29 children in whom the foreign body was located in the trachea or mainstem bronchus. There were eight minor complications, and in three instances it was necessary to repeat the bronchoscopy for retained fragments. In the other 28 children the foreign body was located in the segmental or lobar bronchi, and initial treatment consisted of a program employing inhalation bronchodilators, pulmonary drainage, and thoracic percussion. Treatment was successful (foreign body coughed out) in 18 patients (64%). Of the other 10 children subsequent bronchoscopy was successful in eight and failed in two patients. Of the latter patients, one required bronchotomy, and the other coughed out the foreign body. There were no deaths, major complications, or permanent pulmonary damage in either treatment series.

The clinical spectrum of right Bochdalek's hernia.

Congenital right posterolateral (Bochdalek's) diaphragmatic hernia usually has clinical manifestations different from those of left Bochdalek's hernia; it often masquerades as a pleural effusion, an asymptomatic intrathoracic mass, or an intestinal obstruction. The primary reason for the difference in symptoms is the presence of the liver on the right, which occludes the diaphragmatic defect and permits normal development of the ipsilateral lung. We recommend a transabdominal approach for surgical repair.

Prearterial reversed midgut rotation. A rare congenital anomaly.

A patient with a right-sided descending colon, left-sided ascending colon, and transverse colon in front of the superior mesenteric artery is described. We believe that this is only the second case of "prearterial" reversed midgut rotation existing with normally situated stomach and liver. The best explanation for these relationships seems to be (a) anomalous positioning of the primitive midgut-hindgut junction right of midline; (b) ensuing midgut rotation in a reversed, or clockwise, direction.

Pulmonary artery compression by a giant aortocoronary vein graft aneurysm.

Late failure of saphenous vein aortocoronary bypass grafts is predominantly due to vein graft atherosclerotic disease. Rarely, saphenous vein aortocoronary bypass grafts undergo aneurysmal degeneration. We report a case of a giant true aneurysm of a saphenous vein aortocoronary bypass graft producing right heart failure from main pulmonary artery compression.