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Ann Thorac Surg 2001;72:187-192
© 2001 The Society of Thoracic Surgeons

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Original article: cardiovascular

Cerebral oxygen saturation before congenital heart surgery

Accepted for publication March 2, 2001.

Address reprint requests to Dr Kurth, Department of Anesthesiology, The Children’s Hospital of Philadelphia, 34th St and Civic Center Blvd, Philadelphia, PA 19104
e-mail: kurth{at}email.chop.edu

	Abstract

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Background. In congenital heart disease (CHD), neurologic abnormalities suggestive of hypoxia-ischemia are often apparent before cardiac surgery. To evaluate preoperative cerebral oxygenation, this study determined cerebral O₂ saturation (Sc_O2) in CHD and healthy children.

Methods. Ninety-one CHD and 19 healthy children aged less than 7 years were studied before surgical or radiologic procedures. Arterial saturation (Sa_O2) and Sc_O2 were measured by pulse-oximetry and near infrared cerebral oximetry. Cerebral O₂ extraction (CE_O2) was calculated (Sa_O2-Sc_O2). Sa_O2, Sc_O2, and CE_O2 were compared among diagnoses. Multivariable regression was performed between Sc_O2 and clinical variables.

Results. In healthy subjects, Sc_O2 (68% ± 10%) and CE_O2 (30% ± 11%) were similar to patients with ventricular septal defect, aortic coarctation, and single ventricle after Fontan operation. Sc_O2 was significantly decreased in patients with patent ductus arteriosus (53% ± 8%), tetralogy of Fallot (57% ± 12%), hypoplastic left heart syndrome (46% ± 8%), pulmonary atresia (38% ± 6%), and single ventricle after aortopulmonary shunt (50% ± 7%), or bidirectional Glenn operation (43% ± 6%). CE_O2 was significantly different only in patent ductus arteriosus (46% ± 8%) and hypoplastic left heart syndrome (38% ± 12%). In multivariable regression, only Sa_O2 was related to Sc_O2 (R = 0.63, p < 0.001).

Conclusions. Cerebral oxygenation in CHD varies with anatomy and arterial saturation, and in some patients, it is very low compared with healthy subjects.

	Introduction

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Advances in the care of children born with congenital heart disease (CHD) over the past decade have yielded a dramatic reduction in mortality. Attention is now being directed to the morbidity associated with the disease and its treatment. Of particular concern are the neurologic problems, which afflict 5 to 25% of the survivors, and include diminished cognitive performance, developmental delay, attention deficit hyperactivity disorder, seizures, and cerebral palsy [1–3]. Many of these problems have been attributed to cardiopulmonary bypass (CPB), deep hypothermia, and/or total circulatory arrest (DHCA). However, a growing body of evidence indicates that many neurologic abnormalities originate before surgery [3–6]. The etiology of these abnormalities remains uncertain, although they are suspected in many instances to reflect cerebral hypoxia-ischemia.

Identifying cerebral hypoxia-ischemia in infants with CHD has been difficult. Neurologic examination, electroencephalography, jugular bulb oximetry, and magnetic resonance imaging (MRI) are nonspecific tests or risky procedures to perform in critically ill infants. On the horizon, are noninvasive, bedside, optical technologies such as cerebral oximetry and near infrared spectroscopy (NIRS), which can detect tissue hypoxia-ischemia.

Previous work with NIRS described changes in cerebral oxygenation in neonates, infants, and children undergoing cardiovascular surgery. These studies found cerebral oxygenation to decrease during low flow CPB and DHCA, indicating that certain phases of the surgical procedure put the brain at risk of hypoxic-ischemic injury [7–10]. However, limitations in the technology precluded the determination of cerebral oxygenation before surgery (ie, base line). The technologic advances in the past few years have permitted the determination of base line cerebral oxygenation and investigation of cerebral hypoxia-ischemia before surgery. The present study examined cerebral O₂ saturation (Sc_O2) in neonates, infants, and children with CHD before surgery.

	Material and methods

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Subjects
After Institutional Review Board approval and informed parental consent, we enrolled children aged older than 7 years of age scheduled for cardiac surgical or radiologic procedures. Inclusion criteria included the presence of congenital cardiovascular disease (CHD group), or absence of systemic disease (healthy subjects-Control group). Exclusion criteria were pulmonary, neurologic, or craniofacial disease, history of birth asphyxia, or a genetic abnormality associated with a brain malformation.

Studies were conducted in the cardiac operating room before induction of general anesthesia, or in the radiology sedation suite. All subjects aged older than 6 months received sedative medication before the study, according to our institutional practice. The cardiac surgical premedication consisted of pentobarbital (4 mg/kg PO) for infants 6 months to 1 year, and pentobarbital and meperidine (3 mg/kg PO) for children older than 1 year. The radiologic pre-medication was pentobarbital (2 mg/kg IV). Infants aged less than 6 months did not receive sedative medication.

Cerebral oximetry
NIRS and cerebral oximetry are identical technologies. They rely on the relative transparency of biological tissue to near infrared light (700 to 900 nm) where oxy- and deoxy hemoglobin and cytochrome aa₃ have distinct absorption spectra. By monitoring light signals at several wavelengths, it is possible to determine Sc_O2, concentrations of oxy- and deoxy- hemoglobin, and cytochrome aa₃ redox state [7–13]. At present, the devices are based on continuous-wave or frequency-domain technology. Continuous-wave devices have been available for several years and monitor the intensity of the detected light relative to the emitted light; they describe oxygenation changes over time from an unknown base line [7–10]. Frequency-domain devices are a new technology and monitor intensity as well as phase-shift of the detected light relative to the emitted light; these devices can determine base line oxygenation as well as change over time [11–13]. In this study, Sc_O2 was measured with a prototype frequency domain cerebral oximeter (NIM Incorporated, Philadelphia, PA) [14].

Cerebral oximetry and pulse-oximetry differ in several respects. Although both use near infrared light signals, pulse oximetry monitors the pulsatile signal component reflecting the arterial circulation, whereas cerebral oximetry monitors the nonpulsatile signal component reflecting the tissue circulation (arterioles, capillaries, venules). Cerebral oximetry views a "weighted average" of the tissue circulation, with approximately 85% of the signal originating from venules [11]. Because Sc_O2 is close to venous S_O2, cerebral O₂ extraction (CE_O2) can be estimated from the difference of Sa_O2 and Sc_O2 (CE_O2 = Sa_O2 - Sc_O2). Cerebral oximetry illuminates a "banana-shaped" tissue volume located about 2 cm beneath the optical probe; in young children (age < 7 years), the thin scalp and skull does not interfere [13].

Protocol
The optical probe was held on the forehead below the hairline. Sc_O2 was recorded over one minute while the subject was supine, quiet, and breathing spontaneously or by mechanical ventilation with room air or supplemental inspired O₂, as indicated by the subject’s condition before the study. Sa_O2 (pulse oximetry) and arterial pressure were measured at the same time. Other data were recorded from the medical chart. In the CHD group, outcome was noted as "favorable" or "adverse" for 3 days postoperatively; the latter was defined by the occurrence of clinical seizures, stroke, coma, or death.

Data analysis
Data are presented as mean ± standard deviation. Comparisons between Control and CHD groups were made by analysis of variance (ANOVA) or Fisher’s exact test. When a significant overall F was found in ANOVA, pairwise multiple comparisons were made using Tukey’s test. Spearman’s correlation coefficient was calculated between Sc_O2 and demographic and physiologic variables. The relationship between Sc_O2 and the set of potential predictor variables (defined as those variables correlating with Sc_O2 at the less than or equal to 0.01 level of significance) was explored in a multivariable linear regression model using a forward stepwise variable selection method. When the R² change was less than 0.05, the selection process was terminated. Fischer’s exact test compared favorable and adverse outcomes by preoperative Sc_O2. Statistical significance is p less than 0.05.

	Results

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We enrolled 112 children, 93 in the CHD group and 19 in the Control group. The protocol was completed in 110 subjects; in 2 CHD subjects, neither cerebral or pulse oximetry could be performed (subjects were uncooperative). Table 1 displays the characteristics of the subjects completing the protocol. Of the 91 CHD subjects, 62% were male, 72% were white, and 62% were neonates (< 1 month) or infants (< 12 months). The Control and CHD groups differed in gender (p = 0.044) but not in race (p = 0.36) or age (p = 0.38).

View larger version (14K): [in this window] [in a new window]   Fig 1. Relationship of arterial and cerebral O2 saturation in neonates, infants, and children with congenital heart disease (CHD). (n = 91.)

	Comment

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Neurologic problems occur not uncommonly in CHD [1–3]. They may originate before, during, or after surgery, as a result of cerebral hypoxia, global ischemia, emboli, thrombosis, or genetic defects [3–6, 14, 15]. Our study shows that cerebral oxygenation is low in many patients with CHD, and very low in a few patients, which may represent cerebral hypoxia. Cerebral oxygenation correlated best with Sa_O2. Anatomic diagnosis also influenced it apart from Sa_O2, indicated by CE_O2 in PDA and HLHS. However, the predictive value of Sa_O2 and other clinical factors for cerebral oxygenation was not good. With further work, cerebral oximetry might be used to identify cerebral hypoxia preoperatively, to guide ICU care and timing of surgery.

In the brain, the major source of tissue O₂ content is the saturation of blood in the microcirculation. As a measure of this, Sc_O2 reflects brain tissue O₂ content, which is influenced by cerebral O₂ delivery, O₂ consumption, and arterial/venous blood volume ratio. Because the latter does not differ among CHD lesions [11], the decreased Sc_O2 had to result from altered cerebral O₂ delivery and/or O₂ consumption. Cerebral O₂ delivery is defined by Sa_O2, cerebral blood flow, and hemoglobin concentration. In our study, decreased Sa_O2 was one factor for decreased Sc_O2 in CHD. Hemoglobin concentration, sedation, cardiovascular drugs, mechanical ventilation, and neurologic injury were not factors, because the univariate analysis did not disclose an effect on Sc_O2, and subjects with preoperative neurologic injury were excluded from the study.

The critical Sc_O2 that results in cerebral hypoxic-ischemic damage is uncertain. Preliminary work suggests it occurs in the vicinity of 30% at normothermia, because this Sc_O2 is associated with decreased cerebral energy state, decreased EEG activity, and reduced cytochrome aa₃; physiologic changes that inevitably lead to neuronal necrosis [18, 19]. We observed one neonate to have Sc_O2 below this threshold (incidence 1%). This neonate was lethargic and hypotonic during the preoperative measurement, and had an adverse outcome postoperatively. However, it is possible for neurologic injury to occur following less severe cerebral hypoxia over a longer duration [20]. We observed 12 infants to have Sc_O2 between 31% and 38% (incidence 13%). One of these infants had an adverse outcome (seizures). However, our assessment of neurologic status (history and physical examination) during the preoperative measurement and postoperatively was not sensitive for neurologic injury. Further studies involving neurologic outcome and more sensitive methods to detect cerebral injury are required to define critical Sc_O2 and the value of the technology in this population.

In healthy pediatric and adult humans and animals, CE_O2 is 25 to 40% [21, 22]. We observed most children with CHD to have CE_O2 in this range, as have others [22]. Cerebral blood flow, hemoglobin-O₂ binding affinity (P50), and cerebral metabolic rate influence CE_O2. Noteworthy was the significantly increased CE_O2 in HLHS and PDA. We believe that this reflects decreased cerebral blood flow as a result of diastolic "run-off." [23]

Neurologic problems in CHD are clearly multifactorial in origin. A large body of work has shown neurologic injury can occur from CPB and DHCA [15]. However, the correlation between neurologic injury and duration of CPB and DHCA is weak [1]. Moreover, in animal studies, brain damage does not occur until DHCA is prolonged (> 60 minutes), outside the range of customary clinical practice [16, 17]. These observations point to the important role of factors other than CPB or DHCA in neurologic injury.

Recent work suggests that many neurologic lesions predate surgery. These lesions may be congenital or acquired. McConnell and colleagues observed lesions preoperatively by MRI in 33% of infants, with 95% being acquired and 5% congenital [5]. The majority of acquired lesions were consistent with a global cerebral hypoxia-ischemic insult. In neonates after the arterial switch procedure, Bellinger and associates found that 23% had abnormalities on postoperative MRI, the lesions being acquired in 21% and congenital in 2% [1]. This study confirms the low incidence of congenital lesions, although the incidence of preoperatively acquired lesions was uncertain. However, acquired brain lesions were observed preoperatively by ultrasound in 15 to 20% of young infants with CHD [2, 6].

Neurobehavioral abnormalities also appear commonly before surgery in CHD. Limperopoulos and coworkers observed abnormal neurobehavioral tests in greater than one-half of infants before surgery [4] including hypotonia, hypertonia, altered consciousness, and feeding difficulties. Newberger and associates reported definite abnormalities on neurologic exam in 36% of TGA infants before surgery, a population with a low incidence (2%) of congenital brain lesions [3]. Similarly, Miller and colleagues described hypotonia in 43% of infants with CHD before surgery, well above the incidence of congenital brain malformations (5%) in their population [2]. Taken together, these studies indicate that many infants with CHD have or have had cerebral hypoxia-ischemia before surgery. Our results provide additional evidence to support this hypothesis.

Previous work used NIRS to describe changes in cerebral oxygenation during cardiac surgery. These studies found cerebral oxygenation to decrease during low flow CPB and DHCA, showing that certain phases of the surgical procedure incur a risk of cerebral hypoxic-ischemic injury [7–10]. In addition, CPB hematocrit and pH management was found to influence cerebral oxygenation, indicating that certain strategies might decrease the risk [8, 10]. However, base line cerebral oxygenation before surgery could not be determined with these NIRS instruments. Frequency-domain instruments, an advance in the technology, provide an opportunity to investigate risk before surgery.

Limitations of our study include time- and location sampling bias, as cerebral oxygenation was measured in only one region at one point in time. We attempted to reproduce the subject’s usual resting state at the time of the study. However, Sc_O2 (along with Sa_O2) may vary with time (activity). We examined the frontal neocortex, a region vulnerable to hypoxic-ischemic injury [5, 16], by placing the optical probe on the forehead. However, cerebral oxygenation may differ in another region, reflecting local disease (eg, thrombosis, embolus). Continuous monitoring in more than one location may increase detection of cerebral hypoxia.

Despite decreases in surgical mortality for CHD over the past few decades, neurologic sequelae continue to occur. Surgical factors such as CPB and DHCA have received much attention as contributing factors, and improvements in these techniques have decreased neurologic injury. Our findings add to the evidence suggesting that preoperative cerebral hypoxia-ischemia should now receive more attention.

	Acknowledgments

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This study was supported in part by National Institutes of Health contract N44-NS-5-2314 and NIM Incorporated. The authors thank Paul Gallagher for statistical consultation and Hilary Kleine for help conducting the study.

	References

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 

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