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Ann Thorac Surg 2007;83:1431-1436
© 2007 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Cerebral Oxygen Saturation Does Not Normalize Until After Stage 2 Single Ventricle Palliation

Kathleen N. Fenton, MD*, Katherine Lessman, BS, Kimberly Glogowski, CCP, Sherrie Fogg, CCP, Kim F. Duncan, MD

Department of Surgery, Children’s Hospital, Omaha, Nebraska

Accepted for publication October 3, 2006.

* Address correspondence to Dr Fenton, 14805 Maydale Ct, Silver Spring, MD 20905 (Email: kathleennf{at}msn.com).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background: In an effort to optimize neurologic outcome, cerebral oxygen saturation (ScO 2) is often measured intraoperatively and postoperatively. We hypothesized that ScO 2 would be related to stage of palliation in children with single ventricle congenital heart disease.

Methods: Cerebral oxygen saturation was continuously recorded intraoperatively in 34 infants and children undergoing palliative surgery on cardiopulmonary bypass for single ventricle congenital heart defects and in a control group of 12 neonates with ductus-dependent circulation undergoing complete repair. Saturations were correlated with the patient’s stage and outcome.

Results: Baseline ScO 2 was 61% in single ventricle neonates (group P1, n = 10), 55% in neonates undergoing repair (group R), 42% in infants undergoing stage 2 palliation (group P2, n = 6), and 70% in children undergoing Fontan (group P3, n = 14). Baseline was lowest (41%) in infants undergoing interstage operations (group I, n = 4). After bypass, there was a significant improvement in ScO 2 to 53% in group P2 infants (p = 0.04); there were no significant changes in the other groups. By the end of the operation, there was a significant decrease in ScO 2 to 48% in group P1 (p = 0.001), with other groups unchanged from baseline. There were five perioperative deaths. Cerebral oxygen saturation at the conclusion of surgery was lower in children who died (38% versus 61%, p = 0.01).

Conclusions: In children with single ventricle physiology, ScO 2 decreases after initial palliation, remains low before second-stage palliation, but is normal before and after the Fontan. This has implications for perioperative mortality, neurologic injury, and potentially for interim mortality. Low postoperative ScO 2 predicts perioperative mortality.


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 
Central nervous system (CNS) complications occur in 2% to 25% of children undergoing surgery for congenital heart defects [1, 2]. Neurologic problems identified postoperatively have traditionally been attributed largely to the operation: to periods of hypothermic circulatory arrest, to cardiopulmonary bypass (CPB) itself as well as its complications, and to the edema that is associated with the systemic inflammatory response.

Intraoperative monitoring of the brain has recently been introduced in an effort to detect and correct problems in the operating room. Near-infrared spectroscopy measures the concentrations of oxygenated and deoxygenated hemoglobin and calculates an index of cerebral oxygen saturation (ScO 2). The measurement reflects approximately 75% to 85% cerebral venous blood and has been correlated with jugular vein saturation [3, 4]. The basic principles behind this monitoring technique have been well outlined elsewhere (5–7). Neurologic monitoring during cardiac surgery allows detection and correction of abnormalities in adults [1, 6,8] and children [1, 9], with resultant improvement in outcomes.

Factors other than the adverse effects of surgery may contribute to abnormal neurologic outcome in a significant number of children. Congenital heart defects are common in patients with genetic disorders that are also associated with neurologic abnormality, such as Trisomy 21, Trisomy 18, DiGeorge syndrome, and others.

Other patients with congenital heart defects, but without a recognizable syndrome, also have a higher incidence of CNS malformations. For example, brain abnormalities are associated with coarctation of the aorta, and as many as 30% of infants with hypoplastic left heart syndrome may have brain dysgenesis [1]. Cranial ultrasound images have been shown to be abnormal in 42% of neonates with major congenital heart defects [10]. Cerebral blood flow has also recently been demonstrated to be low preoperatively in infants with congenital heart disease, which correlates with some abnormalities seen on ultrasound images [10]. Finally, although most newborns presenting for cardiac surgery may appear normal to their cardiologists and cardiac surgeons, a careful neurobehavioral evaluation can often identify significant abnormalities, including hypotonia, hypertonia, poor state regulation, and feeding difficulties in more than half [11].

Measurement of cerebral oxygen saturation, in addition to detecting and allowing correction of intraoperative problems, may also have prognostic implications. We [12], and others [2], have recently demonstrated that baseline ScO 2 is related to the cardiac physiology in children undergoing surgery for congenital heart defects. Low baseline ScO 2 was associated with left–right shunt physiology and was a strong predictor of perioperative death in our patient population. Measurement and optimization of ScO 2 may improve outcomes for our highest-risk group of patients, those undergoing staged palliation for single ventricle defects. We hypothesized that ScO 2, a surrogate marker for the adequacy of cerebral (and therefore systemic) perfusion in this patient population, would improve as palliation is accomplished.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 Acknowledgments
 References
 
We retrospectively studied 34 consecutive pediatric patients who underwent staged palliation on CPB for single ventricle congenital heart defects between May 2002 and June 2005 and who had continuous online monitoring of ScO 2 with the INVOS 4100 (Somanetics, Troy, MI) cerebral oximeter. Infants undergoing placement of systemic-to-pulmonary artery shunts without the use of CPB were excluded from this study. The study was reviewed and approved by the Institutional Review Board of Children’s Hospital, Omaha, Nebraska. Individual consent was waived.

Baseline ScO 2 was recorded in the operating room before the induction of anesthesia. Because of the size of the sensors relative to the size of the infant’s forehead, we commonly used only one sensor to measure ScO 2 in infants. The correlation between the two hemispheres in children has been investigated [5]. Because cerebral injury in children is most commonly flow-related, rather than embolic as in adults, we, and others, consider single sensor monitoring to be appropriate. In cases where bihemispheric monitoring was done, we arbitrarily chose to use the value from the right side for the purposes of this study. Because the ScO 2 was continuously recorded, we selected specific time points during the surgery to sample data for analysis. These were noted on the record in the operating room and were consistent across patient groups.

Intraoperative data were recorded into a database prospectively. Preoperative and postoperative data were collected from the patients’ medical records retrospectively. Data were also collected and analyzed for a control group of 12 consecutive newborns with ductus-dependent physiology who underwent complete biventricular repair during the same time period.

Neonates with ductus-dependent circulation were managed with prostaglandin infusion, assessment, and stabilization, followed by repair or palliation at several days of age. The exceptions were 2 infants with infradiaphragmatic total anomalous pulmonary venous connection who were repaired within 24 hours of diagnosis.

Selective cerebral perfusion was routinely used in infants undergoing arch reconstruction. Modified ultrafiltration was routinely used after separation from CPB.

Infants with single ventricle anatomy underwent stage 2 palliation electively at age 3 to 6 months. Completion Fontan was accomplished at 2 to 4 years of age. All children undergoing elective stage 2 or stage 3 palliation had cardiac catheterization before surgery and had pulmonary vascular resistance that was judged by the cardiologist and the surgeon to be satisfactory. The timing of stage 2 and stage 3 palliation was determined by the patient’s systemic oxygen saturation and by the preference of the family and referring cardiologist. An effort made to avoid surgery in the winter months, when possible.

We began using the cerebral oximeter in May 2002, at first sporadically and then routinely for all cardiac procedures. The oximeter was used as a clinical tool in the operating room, and thus, efforts were made to optimize cerebral saturation by adjustments in anesthetic and perfusion techniques, transfusion if indicated, and correction of other identifiable problems.

Patient demographic data were characterized by simple descriptive statistics, including range, mean, and median. Intraoperative cerebral saturation results were compared with baseline in each group using a Student t test. A Student t test was also used to compare ScO 2 in children who died with that in survivors.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 Acknowledgments
 References
 
Patients with single ventricle anatomy were aged 2 days to 71 months (Table 1) and weighed 2.7 kg to 21 kg. Of 22 neonates with ductus-dependent circulation, 12 underwent complete biventricular repair (group R), and 10 underwent stage 1 palliation for single ventricle anatomy (group P1). Initial palliation for these infants included a Norwood operation in 7 (with Sano modification in 5), a central shunt on bypass in 2, and repair of total anomalous pulmonary venous connection with shunt placement in 1 (Fig 1). Repairs included arterial switch operation in 7 neonates, truncus arteriosus repair in 3, and repair of interrupted aortic arch with ventricular septal defect and repair of pulmonary atresia in 1 patient each. Stage 2 palliation was accomplished by a bidirectional Glenn or Hemi-Fontan operation in 6 infants (group P2). Thirteen children (group P3) underwent completion Fontan, 1 of whom underwent reoperation for a baffle leak.


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  		Table 1 Intraoperative Data by Patient Group a
 

Figure 1
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  		Fig 1. Operations for children with single ventricle congenital heart defects.

 
Four patients (group I) with single ventricle physiology had interstage cardiac operations on CPB. All of these were infants who presented with hypoxemia after the initial palliation. One was a 5-month-old former premature infant whose pulmonary vascular resistance was too high to permit stage 2 palliation and who had outgrown his shunt; he underwent placement of an additional shunt. A second infant, with tricuspid atresia, bilateral branch pulmonary artery stenoses, and marginal pulmonary vascular resistance, failed an attempted bidirectional Glenn procedure with bilateral pulmonary artery augmentation and had replacement of a shunt. The third was a 1-month-old infant with heterotaxy syndrome who had undergone a shunt placement and had a persistent oxygen requirement. He was found at cardiac catheterization to have infradiaphragmatic total anomalous pulmonary venous connection and underwent repair. The final infant was 6 weeks old and had an unbalanced complete atrioventricular septal defect and had undergone coarctation repair and pulmonary artery banding as a neonate, and subsequently presented for Damus-Kaye-Stansel palliation.

Mean baseline ScO 2 was 59% (range, 26% to 86%, Table 1) for the entire cohort. Neonates with ductus-dependent circulation had a baseline ScO 2 of 57% (range, 48% to 71%); baseline was 61% in group P1, and 55% in group R (p = NS). Baseline ScO 2 was lowest in infants who had already completed initial palliation: 41% in group I and 42% in group P2. Children presenting for completion Fontan (group P3) had normal baseline ScO 2 (mean, 70%) despite their cyanosis (Table 1).

Cerebral oxygen saturation increased on bypass in all groups (Fig 2), as has been previously reported [2, 4]. After bypass, neonates in group R had a slightly improved ScO 2 (Fig 2), but ScO 2 was slightly lower than preoperatively in group P1. Neither of these changes reached statistical significance. The group P2 infants were the only ones in which there was a significant improvement in ScO 2 immediately after CPB, to 53% (p = 0.04). Normal ScO 2 was maintained in children undergoing completion Fontan. Cerebral oxygen saturation was not affected by modified ultrafiltration (Fig 2). By the time infants in group P1 had left the operating room, however, a significant decrease had occurred in ScO 2 to 48% (p = 0.001). There was no significant change from baseline in the other groups (Table 1), although there was a trend toward a higher ScO 2 in group P3 (p = 0.08).


Figure 2
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  		Fig 2. Intraoperative trends in cerebral oxygen saturation (ScO 2). (Group R, diamonds; group P1, squares; group 1, triangles; group P2, crosses; group P3, scored cross. CPB = cardiopulmonary bypass; MUF = modified ultrafiltration.)

 
Central venous pressure was normal in all infants preoperatively and was increased at the conclusion of the operation only in Fontan patients (Table 2). The hematocrit was significantly increased from its preoperative value in all neonates and in infants in group I (Table 2), reflecting intraoperative transfusion and modified ultrafiltration.


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  		Table 2 Preoperative and Postoperative Central Venous Pressure and Hematocrit in Each Patient Group
 
Significant CNS complications, defined as a temporary or permanent clinical neurologic abnormality, occurred in 7 patients (15%): infarcts in 3, and periventricular ischemia, diffuse edema, atrophy, and seizures in 1 patient each. In this small study, there was no relationship between ScO 2 and CNS complications (Table 3).


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  		Table 3 Relationship of Intraoperative Indicators to Central Nervous System Complications
 
There were five perioperative deaths (11%), all in single ventricle patients. Three were in group P1: two after stage 1 palliation for hypoplastic left heart syndrome (one with Sano), and one after shunt placement. One infant in group P2 died, and the final death was the previously mentioned group I infant who failed stage 2 palliation and was converted back to a shunt. Cerebral oxygen saturation at the conclusion of the operation was lower in infants who died perioperatively (38% versus 61%, p = 0.01, Fig 3). There were three late deaths: one each after truncus arteriosus repair, hemi-Fontan, and Damus-Kaye-Stansel palliation. There was no relationship between intraoperative ScO 2 and late mortality. Overall (early and late) mortality for group I was 75%.


Figure 3
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  		Fig 3. Relationship of cerebral oxygen saturation (ScO 2) to perioperative mortality. (Alive, filled bars; late death, diagonal fill; early death, diamond fill. CPB = cardiopulmonary bypass.)

 

   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
Acknowledgments
 References
 
Children, and particularly infants undergoing repair of congenital heart defects, remain at high risk of both death and neurologic injury. Attempts to improve neurologic outcome have included avoiding or minimizing the use of deep hypothermic circulatory arrest and, more recently, intraoperative brain monitoring using transcranial Doppler ultrasound, electroencephalogram, and cerebral oximetry. At the same time, a growing body of evidence suggests that infants with congenital heart disease do not begin postnatal life with a normal brain [1, 2, 10, 11] and that diminished cerebral blood flow preoperatively may contribute significantly to adverse outcome [10, 11]. All of this means that we are going to the operating room with a child that is at high risk of neurologic injury not only because of the heart defect but also because of preexisting neurologic abnormalities.

In this study, we set out to evaluate the relationship between the stage of repair (physiology) and ScO 2 in children with single ventricle congenital heart disease. These children have significant changes in cardiovascular physiology as staged palliation is accomplished. Neonates with ductus-dependent circulation have a physiology that is characterized by mixing of oxygenated and deoxygenated blood (cyanosis) as well as significant pulmonary overcirculation with its attendant volume load on the heart. In cases in which complete repair is possible, postoperative physiology is "normal" (that is, no left-to-right shunt and no mixing or cyanosis), but infants undergoing stage 1 palliation are left with the same physiologic abnormalities, plus those added by surgery and CPB. Even when the right ventricle–pulmonary artery conduit is used, the pulmonary–systemic flow ratio remains significantly higher than 1:1.

Stage 2 palliation is designed to get rid of the pulmonary overcirculation, but the child is left with the physiology of mixing and now has an added resistance load on the single ventricle.

Finally, after the Fontan, the child has no mixing, no cyanosis, and no extra volume load on the heart, but the single ventricle faces the physiologic challenge of pumping against two serial resistance circuits.

We have shown that ScO 2, measured in the operating room, is related to the stage of palliation (the cardiovascular physiology). Baseline ScO 2 for various congenital heart defects has been previously reported by us [12] and others [2]. This study has specifically evaluated the changes in ScO 2 during the various stages of single ventricle palliation.

Neonates with ductus-dependent circulation have, on average, a lower-than-normal ScO 2, but this difference does not reach significance in this small study. These infants are struggling with a physiology of high cardiac output and high pulmonary blood flow. After bypass, ScO 2 is higher in repaired infants (group R), but it trends downward in those who are palliated (group P1); at the conclusion of surgery, ScO 2 was significantly lower than baseline in group P1. This most likely reflects the underlying physiology, which has been corrected only in the first group.

Low ScO 2 has been previously reported in neonates after Norwood palliation [13]. Infants undergoing stage 1 palliation are left with both cyanosis from mixing and left–right shunt physiology, which results in a combination of lower arterial and lower mixed venous oxygen saturation, both contributing to decrease ScO 2. Initial palliation may limit pulmonary blood flow but does not alter the underlying physiology. It might therefore be expected to stabilize—but not greatly "improve"—systemic perfusion and ScO 2, relative to the infant with an open ductus arteriosus.

Group I infants had the lowest baseline ScO 2 of the cohort. We may be able to explain this from their physiology: a combination of the inherently inefficient stage 1 physiology that is now exacerbated by progressive systemic cyanosis. Infants presenting for stage 2 palliation similarly had relatively low baseline ScO 2. Group I infants were subjected to the stress of a second palliative operation that did not change their underlying physiology of high cardiac output, elevated pulmonary blood flow, and mixing, so it may come as no surprise that their ScO 2 did not improve postoperatively, despite an improvement in the arterial partial pressure of oxygen (Table 2). Similarly, it is this group that had the highest mortality.

Although infants undergoing stage 2 palliation often do not have any improvement in systemic oxygen saturation after surgery, we might expect their ScO 2 to be higher postoperatively owing to the improved physiology (with resultant higher mixed venous saturation). Our data support this assessment of the physiology: Group P2 infants left the operating room with ScO 2 significantly higher than baseline, despite no significant differences in arterial oxygen saturation, central venous pressure, or hematocrit. This is especially noteworthy when one considers that these values are measured shortly after CPB, at which time the infant would be expected to have some degree of bypass-related decrement in oxygenation; the data may therefore under-represent the patient’s actual stage 2 physiology. This hypothesis is supported by the fact that ScO 2 improves over time and normalizes before the Fontan.

Children undergoing completion Fontan had normal ScO 2 before, during, and after surgery, with a trend towards higher saturation at the end of the operation, possibly reflecting the higher systemic oxygen saturation.

We did not demonstrate a relationship between perioperative CNS complications and low ScO 2. This is partly related to the size of the study but may also be influenced by the fact that ScO 2 was used as a clinical tool in our patients and every effort was made to optimize it. Perioperative neurologic injury, therefore, resulted from causes unrecognized by our monitoring (ScO 2 was normal) or from physiologic problems that we were unable to rectify. It is important to emphasize that neurologic complications can and do occur in patients with normal ScO 2 and that monitoring a normal ScO 2 should not be taken as assurance that no CNS complications will occur.

The overall perioperative mortality in our study was 11%, with the highest mortality in the patients undergoing interstage operations (25%) and those undergoing stage 1 palliation for hypoplastic left heart syndrome (22%). These results are comparable with recent studies of single ventricle palliation in similarly sized programs [14–18]. We have previously demonstrated that an abnormally low baseline ScO 2 is predictive of perioperative death in a larger cohort of children undergoing repairs for congenital heart disease [12]. In the current smaller study we were able to demonstrate a strong correlation between low postrepair ScO 2 and perioperative death. Presumably this correlation would have been even stronger had we made no attempt to correct the low ScO 2.

In most of our patients, ScO 2 is most likely a surrogate marker for systemic perfusion; it has been shown elsewhere [7] to correlate with mixed venous oxygen saturation in children undergoing cardiac surgery. Continuous monitoring of ScO 2, like mixed venous oxygen saturation allows early recognition of the fact that "something" is wrong and permits early intervention.

The significant drop in ScO 2 after initial palliation is especially concerning in view of the high mortality rate between the first and second stages of single ventricle palliation [15, 19, 20]. It may very well be that patients who leave the operating room, the intensive care unit, or the hospital with low ScO 2 are at higher risk of interim death. It may also be that monitoring ScO 2 intermittently on an outpatient basis may allow earlier detection, and thus correction, of physiologic problems.

Limitations of our study include its small size and generally retrospective design. The hemodynamic data from the patient’s preoperative cardiac catheterization was temporally too far removed from the operation to provide usable data. Similarly, it would be helpful to report hematocrit and systemic arterial oxygen saturation values sampled at the same time as the ScO 2, but we are unable to exactly correlate the timing of the respective samples. Another limitation is that it does not include all of the patients who underwent surgery during the study period because the oximeter was at first used only sporadically.

A longitudinal study, with evaluation of the same patient population progressing through staged palliation, may have provided additional information but would have had the disadvantage of magnifying the effects of changes in practice pattern over time. Finally, although we determined that ductus-dependent neonates undergoing a complete two-ventricle repair made a good comparison group for those undergoing initial palliation, we were unable to find satisfactory "control" groups for stages 2 and 3.

Future work in this area might include the use of ScO 2 measurement to better evaluate how to optimize physiology in patients during and after initial palliation. For example, how does use of the Sano modification affect cerebral oxygenation, and what is the optimum conduit size? Will monitoring ScO 2 after surgery, in the intensive care unit or sporadically on an outpatient basis, allow detection of problems with a resultant improvement in outcome? It might also be interesting to attempt to correlate ScO 2 with more subtle neurologic abnormalities by formal neurologic evaluation.

In conclusion, we have demonstrated that initial palliation of single ventricle congenital heart disease results in a significant decrease in ScO 2 that is not seen in neonates undergoing complete two-ventricle repair. This low ScO 2 persists over time (stage 2 infants have the lowest baseline ScO 2) and we speculate that it may correlate with interim mortality. Low postoperative ScO 2 is related to perioperative mortality in children undergoing palliation of single ventricle congenital heart disease.


   Acknowledgments
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
References
 
We would like to acknowledge the collaboration of Kimberly Hanson, MD, Donald Felix, MD, Joseph Deptula, CCP, Kellie Merrigan, CCP, and Marilyn Carlson.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Andropoulos DB, Stayer SA, Diaz LK, Ramamoorthy C. Neurological monitoring for congenital heart surgery Anesth Analg 2004;99:1365-1375.[Abstract/Free Full Text]
  2. Kurth CD, Steven JL, Montenegro LM, et al. Cerebral oxygen saturation before congenital heart surgery Ann Thorac Surg 2001;72:187-192.[Abstract/Free Full Text]
  3. Abdul-Khaliq H, Troizsch D, Schubert S, et al. Cerebral oxygen monitoring during neonatal cardiopulmonary bypass and deep hypothermic circulatory arrest Thorac Cardiov Surg 2002;50:77-81.
  4. Daubeney PEF, Smith DC, Pilkington SN, et al. Cerebral oxygenation during paediatric cardiac surgery: identification of vulnerable periods using near infrared spectroscopy Eur J Cardiothorac Surg 1998;13:370-377.[Medline]
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  7. Tortoriello TA, Stayer SA, Mott AR, et al. A noninvasive estimation of mixed venous oxygen saturation using near-infrared spectroscopy by cerebral oximetry in pediatric cardiac surgery patients Paediatr Anaesth 2005;15:495-503.[Medline]
  8. Edmonds HL. Multi-modality neurophysiologic monitoring for cardiac surgery Heart Surg Forum 2002;5:225-228.[Medline]
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  10. Te Pas AB, van Wezel-Meijler G, Bokenkamp-Gramann R, Walther FJ. Preoperative cranial ultrasound findings in infants with major congenital heart disease Acta Paediatrica 2005;94:1597-1603.[Medline]
  11. Limperopoulos C, Majnemer A, Shevell MI, et al. Neurologic status of newborns with congenital heart defects before open heart surgery Pediatr 1999;103:402-408.[Abstract/Free Full Text]
  12. Fenton KN, Freeman K, Glogowski K, Fogg S, Duncan KF. The significance of baseline cerebral oxygen saturation in children undergoing congenital heart surgery Am J Surgery 2005;190:260-263.[Medline]
  13. Hoffman GM, Stuth EA, Jaquiss RD, et al. Changes in cerebral and somatic oxygenation during stage 1 palliation of hypoplastic left heart syndrome using continuous regional cerebral perfusion J Thorac Cardiovasc Surg 2004;127:223-233.[Abstract/Free Full Text]
  14. Checchia PA, McCollegan J, Daher N, et al. The effect of surgical case volume on outcome after the Norwood procedure J Thorac Cardiovasc Surg 2005;129:754-759.[Abstract/Free Full Text]
  15. Cua CL, Thiagarajan RR, Taeed R, et al. Improved interstage mortality with the modified Norwood procedure: a meta-analysis Ann Thorac Surg 2005;80:44-49.[Abstract/Free Full Text]
  16. Krasemann T, Fenge H, Kehl H-G, et al. A decade of staged Norwood palliation in hypoplastic left heart syndrome in a midsized cardiosurgical center Pediatr Cardiol 2005;26:751-755.[Medline]
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