Asian Cardiovasc Thorac Ann 2008;16:115-119
© 2008 Asia Publishing EXchange Ltd
Survival after Surgery with Cardiopulmonary Bypass in Low Weight Patients
Takashi Miyamoto, MD,
Nicodème Sinzobahamvya, MD,
Joachim Photiadis, MD,
Anne M Brecher, MD,
Boulos Asfour, MD
Department of Pediatric Cardiothoracic Surgery, German Pediatric Heart Center, St. Augustin, Germany
For reprint information contact: Takashi Miyamoto, MD, Tel: 81 279 523 511, Fax: 81 279 522 045, Email: yonomiyataka{at}msn.com, Department of Cardiovascular Surgery, Gunma Childrens Medical Center, 779, Shimohakoda, Hokkitsu, Shibukawa, Gunma, 377-8577, Japan.
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ABSTRACT
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To evaluate risk factors for hospital death in patients weighing < 2.5 kg undergoing open-heart surgery, records of 34 consecutive low-weight patients operated on between December 1997 and November 2004 were reviewed. Mean weight was 2.152 ± 0.237 kg (range, 1.600 to 2.460 kg). Biventricular repair was achieved in 28 patients. The most frequent procedures were the arterial switch operation in 9 children, ventricular septal defect closure in 6, repair of total anomalous pulmonary venous connection in 5 and truncus arteriosus repair in 5. There were 8 early deaths. Mortality was strongly associated with the Comprehensive Aristotle Complexity Score: mortality was low (2/27; 7.4%) with a score < 19, and high (6/7; 85.7%) with a score
19. Higher mortality was encountered after univentricular repair (4/6; 67%). Hyperlactatemia at the end of cardiopulmonary bypass was also associated with poor survival. A Comprehensive Aristotle score < 19 was the strongest predictor of survival in low-weight patients undergoing open-heart surgery. Biventricular repair, when feasible, should be promoted to improve outcome.
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INTRODUCTION
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Although the outcome of neonatal cardiac surgery has dramatically improved in the last decades, low body weight still constitutes an important risk factor for morbidity and mortality. Studies have suggested that gestational age and low weight are risk factors for poor outcome of cardiac operations with cardiopulmonary bypass (CPB) for many congenital heart diseases.1,2 Mortality rates in infants < 2.5 kg are high, ranging from 10% to 25%.3,4 There is frequently a delay in definitive surgical repair when a premature or low birth weight infant is found to have symptomatic congenital heart disease. Intensive medical therapy and prolonged continuous prostaglandin infusion in neonates who benefit from ductus patency may guarantee clinical stability with the rationale of delaying surgery. Nevertheless, this strategy does not seem to be associated with better surgical results. Recently, evaluation of the quality of care has become a duty of modern medical practice. The Aristotle system allows simple electronic collection of known complexity factors.5 This should help to collect, analyze and compare data, thus identify and weigh the risk factors. We reviewed our experience of open-heart surgery in low-weight patients and assessed the predictors of postoperative mortality.
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PATIENTS AND METHODS
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From December 1997 to November 2004, 34 consecutive low-weight (< 2.5 kg) patients underwent cardiac surgery with CPB in our center. Preoperative and operative data were retrospectively collected by reviewing the hospital records. The following variables were analyzed as risk factors for early mortality: weight and age at operation, sex, gestational age, prenatal diagnosis, mechanical ventilation, preoperative lactate level, Comprehensive Aristotle Complexity Score, type of surgery (correction or palliation), use of deep hypothermia with circulatory arrest, CPB and cross clamp times, and lactate level at the end of CPB. The Aristotle score, final Nov 30 2004 version (Aristotle Institute, Denver, CO, USA; available at: http://www.aristotleinstitute.org) was used to estimate Comprehensive Aristotle scores. The demographic characteristics of the patients are summarized in Table 1
. Ten (29%) patients weighed
2 kg at operation, and 22 (65%) presented in decompensated cardiac failure. A prenatal cardiac diagnosis had been made in 8 (24%) cases. Preoperatively, all patients were symptomatic, 1 had sepsis, 2 had necrotizing enterocolitis, but none had intraventricular hemorrhage. Correction of metabolic and hemodynamic dysfunction required intravenous prostaglandins for duct-dependent lesions, atrial balloon septostomy in transposition complexes, and administration of inotropic agents and diuretics as needed.
Surgical procedures included the arterial switch operation in 9 patients, ventricular septal defect closure in 6, total anomalous pulmonary venous connection repair in 5, truncus arteriosus repair with a homograft in 5, intraventricular repair of double-outlet right ventricle with closure of aortopulmonary window in 2, aortic valvotomy of critical stenosis in 2, construction of a modified Blalock-Taussig shunt in 2, correction of tetralogy of Fallot in 1, stage I Norwood operation in 1, and atrial septal defect creation and pulmonary artery banding in 1. A palliative procedure was carried out in 6 children. Associated noncardiac malformations or syndromes were present in 5 (15%) patients: asplenia syndrome in 2, DiGeorge syndrome in 2, and Williams-Beuren syndrome in 1. Primary complete repair was achieved in 28 patients, and univentricular palliation in 6. Standard techniques of CPB were used. Pump flow was adjusted to maintain blood pressure
30 mm Hg and left atrial pressure
5 mm Hg (monitored continuously). Intermittent cold crystalloid cardioplegia (St. Thomas Hospital no. 2) solution was administered antegradely into the aortic root or coronary ostia. During CPB, blood gas analysis was achieved using the alpha-stat method. Modified ultrafiltration was carried out after CPB in each patient. Deep hypothermia (18°C) with circulatory arrest was applied in 17 cases; the duration ranged from 5 to 89 min. Cardiopulmonary bypass and aortic cross clamp times were 200 ± 104 min and 61 ± 34 min, respectively. The endpoint was hospital mortality (< 30 days after the operation).
Data are expressed as median and range or mean ± standard deviation, unless otherwise specified. Comparisons of means between groups were performed with the independent samples t test, and comparisons of dichotomous variables between groups were carried out by chi-squared analysis. Statistical analysis was undertaken using SPSS for Windows 6.01 (SPSS Inc, Chicago, IL, USA). A p value < 0.05 was considered statistically signifiant.
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RESULTS
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There were 8 hospital deaths (4 after definitive correction and 4 after univentricular palliation), giving a hospital mortality rate of 23.5%. Table 2
lists details of the patients who died; death was due to cardiogenic shock in 3, intractable pulmonary hypertension in 4 and shunt failure in 1. All 3 deaths in infants with total anomalous pulmonary venous connection were due to irreversible pulmonary hypertension. Of the 4 patients who underwent univentricular repair, 2 had total anomalous pulmonary venous connection with single ventricle. Another was case no. 1 (Table 2
) which was converted to the Norwood procedure immediately after failure of biventricular repair for a hypoplastic left heart complex lesion. The 4th patient had shunt thrombosis related to unfavorable anatomy of the pulmonary arteries. As shown in Table 3
, variables associated with high early mortality were high Aristotle score, type of repair (with higher mortality after univentricular repair), and high lactate levels (
5 mmolL–1) at the end of CPB. Mortality strongly correlated with Aristotle scores (Table 4
, Figure 1
), increasing from 14% at level 4 to 50% at level 6, survival being exceptional when the score reached 19 (mortality, 85.7%).
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DISCUSSION
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In addition to the usual shortcomings of a retrospective study, this study was hampered by the small number of patients and the methodology used to estimate lactate levels. These are known to vary with time, and only mean values are given here, thus the results for this parameter have to be considered with caution.
Although the outcome of surgical correction of cardiac lesions has dramatically improved in the last decade, the risk of open-heart surgery in the neonatal period remains substantial, with an operative mortality in the order of 10%.6,7 This is due to greater complexity of lesions that dictate early intervention, and to the more marked deleterious effects of extracorporeal circulation in newborns. Thus, higher mortality should be expected in premature and low-weight infants undergoing open-heart surgery. Some specific problems may be highlighted: inadequate maturation of organ systems; poor homeostasis with rapid changes in pH, lactate, glucose and temperature; underdevelopment of the myocardium which is less compliant, less tolerant to increased afterload and less responsive to increased preload; pulmonary disease such as apnea, hyaline membrane disease and bronchopulmonary dysplasia; and increased tendency to suffer necrotizing enterocolitis and renal insufficiency.8,9
In previous reports, risk factors for early mortality after open-heart surgery in patients weighing < 2.5 kg were perioperative metabolic acidosis, univentricular palliation, duration of CPB, prolonged circulatory arrest and postoperative low cardiac output.2,10 This study identified Comprehensive Aristotle score
19, univentricular palliation and lactate level
5 mmolL–1 at the end of CPB as adverse factors for early survival. Aristotle scoring is still under validation, and it should be noted that weight < 2.5 kg and prematurity are recorded as general independent factors with 2–4 points in the scoring system.5,6 There are currently few reports on the Comprehensive Aristotle score for comparison, but 3 have shown that hospital mortality correlates with higher Aristotle scores, with a very low survival rate when the score reaches 20 to 25.11–13 The threshold in this study was a score of 19; below this cut-off point, operative risk was low (7.4%), whereas at
19, mortality was excessive (85.7%).
Cardiopulmonary bypass in patients with univentricular hearts was found to be associated with a higher early mortality than in those with 2 ventricles. The outcome in such patients is determined by the interplay of various factors including the morphology of the single systemic ventricle, competence of the atrioventricular valves and associated subaortic obstruction, pulmonary vascular resistance and difficulty in balancing the pulmonary and the systemic flows. Weight < 2.5 kg constitutes an additional hazard. This was demonstrated particularly for the Norwood stage I operation, the most frequent univentricular palliative procedure in the neonatal period.13 Our study confirms this incremental risk, with 67% operative mortality. It should be noted that 50% of these univentricular cases had Aristotle scores
19. High serum lactate levels during CPB and increasing hyperlactatemia in the first 24 hours after congenital cardiac surgery have been reported to be major predictors of early mortality, the threshold being 3–4 mmolL–1.14–16 In this study, the crucial level was 5 mmolL–1, but as discussed above, this should be accepted with reservation. Interestingly, the duration of circulatory arrest, which is associated with increased lactate levels, was not found to be a significant risk factor.
It was concluded that Aristotle score
19 is the strongest predictor of death after open-heart surgery in patients weighing < 2.5 kg, and univentricular palliation is the 2nd strongest risk factor. Accordingly, to improve outcome, efforts should be devoted preoperatively to manage procedure-independent factors that increase the patient-adjusted complexity score, and thus the Comprehensive Aristotle score.5,6 Early referral, stabilization of the patient and timing of the intervention (no undue delay) carry the potential for outcome improvement. Biventricular repair, when feasible, should be promoted. Surgical techniques avoiding circulatory arrest and allowing surgery on a beating heart should be considered for high-risk (Aristotle score
19) patients. Postoperatively, the threshold to start extracorporeal membrane oxygenator support should be lowered, particularly in the case of increasing lactate levels despite adequate management.
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