THERAPEUTIC STRATEGIES IN REFRACTORY LOW-CARDIAC-OUTPUT SYNDROME IN NEWBORNS AND CHILDREN

A refractory low-cardiac-output syndrome is, in pediatric patients, most often due to impaired myocardial function after corrective surgery in congenital heart disease. Therapy has to focus on postoperative adaptation, which usually takes place within a few days. We report on three therapeutic strategies to ''bridge'' this phase of postoperative adaptation. Improving the contractile state of the myocardium using enoximone was attempted in 16 neonates with low-cardiac-output syndrome refractory to catecholamines (Dosage: loading-dose 1 mg/kg in 10 min intravenously, followed by an infusion of 10 mcg/kg/min). In 12/16 neonates cardiac index increased by more than 20 % (''responder''), while in 4/16 neonates cardiac index remained unchanged (''non-responder''). All non-responders succumbed due to refractory low-cardiac-output syndrome, while only one responder died in low-cardiac-output syndrome. Hemodynamically, enoximone resulted in an increase of cardiac index and stroke volume (p < 0.003), a reduced systemic vascular resistance (p < 0.0022), and reduced right and left atrial pressures (p < 0.003). Heart rate and mean arterial pressure remained unchanged. No rhythm disturbances were observed. Another therapeutic approach to postoperative low-cardiac-output syndrome is atrial decompression by creating an atrial septal defect. Due to the possibility of later transcatheter closure of these defects, the acceptance for the intraoperative creation of an atrial communication to decompress the right or left atrium is increased. The defect size is critical and should be below 9 mm, so that the Rashkind-PDA-Occluder can be used for later transcatheter closure. We performed such a ''surgical-interventional'' decompression in 18 patients (age : 2 weeks to 7 years). In six patients the atrial defect was created because of an underdeveloped left ventricle (body weight 2,9-9,2 kg), in 12 patients for right atrial decompression during a total cavopulmonary shunt (body weight 15.2-54.2 kg). A spontaneous closure of the defect did not occurred in any of the patients, thus, transvenous closure of the defect was performed 2 to 10 weeks postoperatively. In the follow-up period of 4 to 22 months no complications such as thrombus formation, thromboembolic events or infections occurred. In low-cardiac-output syndrome refractory to all therapeutic measures mechanical circulatory support is the final method to keep the patient alive. In 11 children with refractory low-cardiac-output syndrome mechanical circulatory support was performed. In three of these, extracorporal membrane oxygenation (ECMO) was used, in eight children a ventricular assist device (Berlin Heart) was used. The age ranged from 2 weeks to 16 years (mean 8.5 years). In none of the patients did ventricular function normalize during the assisted circulation. Thus, circulatory support was performed as a bridge to transplant for a duration of 2 to 71 days (mean 16.3 days). Cardiac transplantation was performed in eight patients; five of these survived, while two who were transplanted died of early transplant failure. Persisting multiorgan failure despite adequate circulatory support was observed in three patients; it can be speculated that circulatory support was started too late in these patients.