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ORIGINAL ARTICLE Table of Contents   
Year : 2009  |  Volume : 12  |  Issue : 1  |  Page : 17-0
Changes in near infrared spectroscopy during deep hypothermic circulatory arrest


1 Department of Anesthesiology and Pediatrics, University of Missouri, Columbia, Missouri, USA
2 Department of Pediatrics and Cardiothoracic Surgery, University of Missouri, Columbia, Missouri, USA
3 Department of Nursing, University of Missouri, Columbia, Missouri, USA

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Date of Submission01-Jul-2008
Date of Acceptance10-Sep-2008
 

   Abstract 

Monitoring cerebral oxygenation with near infrared spectroscopy may identify periods of cerebral desaturation and thereby the patients at risk for perioperative neurocognitive issues. Data regarding the performance of near infrared spectroscopy monitoring during deep hypothermic circulatory arrest are limited. The current study presents data regarding use of a commercially available near infrared spectroscopy monitor during deep hypothermic circulatory arrest in paediatric patients undergoing surgery for congenital heart disease. The cohort included 8 patients, 2 weeks to 6 months of age, who required deep hypothermic circulatory arrest for repair of congenital heart disease. The baseline cerebral oxygenation was 63 ± 11% and increased to 88 ± 7% after 15 min of cooling to a nasopharyngeal temperature of 17-18°C on cardiopulmonary bypass. In 5 of 8 patients, the cerebral oxygenation value had achieved its peak value (either ≥90% or no change during the last 2-3 min of cooling on cardiopulmonary bypass). In the remaining 3 patients, additional time on cardiopulmonary bypass was required to achieve a maximum cerebral oxygenation value. The duration of deep hypothermic circulatory arrest varied from 36 to 61 min (43.4 ± 8 min). After the onset of deep hypothermic circulatory arrest, there was an incremental decrease in cerebral oxygenation to a low value of 53 ± 11%. The greatest decrease occurred during the initial 5 min of deep hypothermic circulatory arrest (9 ± 3%). Over the entire period of deep hypothermic circulatory arrest, there was an average decrease in the cerebral oxygenation value of 0.9% per min (range of 0.5 to 1.6% decline per minute). During cardiopulmonary bypass, cooling and deep hypothermic circulatory arrest, near infrared spectroscopy monitoring followed the clinically expected parameters. Such monitoring may be useful to identify patients who have not achieved the highest possible cerebral oxygenation value despite 15 min of cooling on cardiopulmonary bypass. Future studies are needed to define the cerebral oxygenation value at which neurological damage occurs and if interventions to correct the decreased cerebral oxygenation will improve perioperative outcomes.

Keywords: Cerebral oximetry, cerebral oxygenation, near infrared spectroscopy

How to cite this article:
Tobias JD, Russo P, Russo J. Changes in near infrared spectroscopy during deep hypothermic circulatory arrest. Ann Card Anaesth 2009;12:17

How to cite this URL:
Tobias JD, Russo P, Russo J. Changes in near infrared spectroscopy during deep hypothermic circulatory arrest. Ann Card Anaesth [serial online] 2009 [cited 2020 Aug 5];12:17. Available from: http://www.annals.in/text.asp?2009/12/1/17/43057



   Introduction Top


For the correction of specific types of congenital heart disease (CHD), cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA) may be employed to optimise surgical visualisation and allow for the completion of complex repairs. The technique provides the surgeon a bloodless field that is not obstructed by vascular clamps and CPB cannulae. Despite its efficacy in allowing the completion of complex surgical procedures, especially in neonates, neurological sequelae have been recognised and are thought to be dependent on the duration of the DHCA. [1],[2],[3] Methods to limit the adverse neurological impact of DHCA have primarily included hypothermia with core and topical cooling and whenever feasible, the limitation of the duration of DHCA. [4],[5]

The potential use of near infrared spectroscopy (NIRS), otherwise known as cerebral oximetry, to monitor cerebral oxygenation was first suggested by Jobsis in 1977. [6] NIRS is a non-invasive device that uses infrared light to penetrate living tissue like pulse oximetry. The Beer-Lambert law has been used for many years in colorimetric analysis to determine the concentration of a compound in a solution. Light passing through a solution of a coloured compound (chromophores or haemoglobin species) is absorbed by that compound, and therefore, the light emerging from the other side is reduced. The relationship between the light that enters that solution and that exits from it depends on the concentration of the chromophore, its extinction coefficient (the optical characteristics of the compound at specific wavelengths of light), and the thickness of the solution. By use of these principles, the NIRS monitor is able to provide an estimation of brain tissue oxygenation. Unlike standard pulse oximetry, pulsatile flow is not required, and therefore, the device works during CPB and other non-pulsatile states. There has been increased interest in the use of this technology in the perioperative period and in the ICU, especially in the paediatric cardiac surgical population. [7] However, there are limited data regarding its use in patients undergoing DHCA. We present data regarding the performance of NIRS prior to and after the institution of DHCA in a cohort of infants and children.


   Materials and Methods Top


This study involved a retrospective review of quality assurance data that was prospectively collected following the introduction of NIRS monitoring in our paediatric cardiac surgical population. This review and preparation of this manuscript was approved by the hospital's Institutional Review Board. Cerebral oximetry (rSO 2 ) was monitored using a commercially available NIRS monitor (Somanetics INVOS system, Somanetics Inc. Troy, MI). Bilateral paediatric probes placed on the patient's forehead, 0.5-1 cm above the eyebrow with the medial aspect of the probe at the midline of the forehead [Figure 1] and [Figure 2]. The probes were placed after the induction of general anaesthesia and endotracheal intubation. Following placement, the values were recorded every minute by a disk drive attached to the monitor. All patients were also monitored with the bispectral index monitor (BIS monitor, Aspect Medical, Newton, MA) to ensure that a burst suppression pattern had been achieved prior to the institution of DHCA. General anaesthesia consisted of a combination of fentanyl (20-25 µg/kg) and desflurane, which was administered from either the vaporiser on the anaesthesia machine or from the CPB machine. The expired desflurane concentration was titrated according to the patient's haemodynamic status. Neuromuscular blockade was provided by intermittent doses of cis-atracurium.

Technique of CPB and cooling

Following sternotomy and cannulation, CPB was instituted using a non-pulsatile pump flow. The patients were then cooled to a nasopharyngeal temperature of 16-18°C using both surface and core cooling. Surface cooling started after the induction of general anaesthesia and was continued throughout until rewarming was started. Surface cooling included a room temperature of 4-5°C, a cooling blanket set at 4°C, and ice bags placed around the patients' head. Core cooling began with the institution of CPB by setting the water temperature of the heat exchanger at 4-5°C until a nasopharyngeal temperature of 16-18°C was achieved. Blood gas management during cooling was adjusted to maintain a pH of 7.40 with partial pressure of carbon dioxide in arterial blood (PaCO 2 ) of 40 mmHg corrected for body temperature (pH stat). When needed, carbon dioxide (CO 2 ) was added to the gas flow of the oxygenator to achieve the appropriate PaCO 2 . Haemoglobin was maintained at 8-10 gm/dL during CPB. The patients were cooled for at least 15 min. At that time, if the rSO 2 had not reached its optimal value defined as ≥90% on both sides or a peak value as indicated by no change for 3 consecutive minutes, cooling was continued. Prior to the start of DHCA, the blood gas management was changed to the a-stat method.

Data collection

Demographic and baseline data included age, weight, gender, underlying CHD, surgical procedure, baseline cerebral oximetry values (obtained after the induction of general anaesthesia and endotracheal intubation), and the duration of DHCA. The time to achieve the optimal rSO 2 and the number of patients who had not achieved the peak value after 15 min of cooling was determined. The maximum rSO 2 that was achieved prior to the onset of DHCA, the incremental decline in the rSO 2 during DHCA, and the nadir of the rSO 2 values at the completion of DHCA were determined. The data are presented as the mean ± SD. The rSO 2 values were rounded to the nearest whole integer.


   Results Top


The cohort for the study included 8 patients who ranged in age from 2 weeks to 6 months (3 ± 1.7 months) and in weight from 3.7 to 5.2 kg (4.6 ± 0.5 kg) [Table 1]. There were 5 boys and 3 girls. As no difference was noted between the right- and left-sided rSO 2 values, the data were combined to give a single global value. The baseline rSO 2 was 63 ± 11%, increased to 88 ± 7% prior to the onset of DHCA, and then decreased to a low value of 53 ± 11% at the conclusion of DHCA. In all the patients, cooling on CPB was performed for at least 15 min. The nasopharyngeal temperature at the end of 15 min of cooling was 17.1 ± 4°C. The bispectral index monitor revealed a burst suppression pattern in all 8 patients with a BIS value less than 10 and a suppression ratio of ≥ 85%. In 5 of 8 patients, the rSO 2 had achieved its maximal possible value (either ≥ 90% or no change during 2-3 min of cooling on CPB) after 15 min. In the remaining 3 patients, additional time cooling on CPB was required to achieve a maximum NIRS value. Additional cooling was required for an additional 5, 7, and 8 min in these 3 patients. There was no difference in the nasopharyngeal temperature in these 3 patients compared to the other 5 patients (17.2 ± 0.5 vs. 17.1 ± 0.4). The duration of DHCA varied from 36 to 61 min (43.4 ± 8 minutes) for a total DHCA time of 347 min in the 8 patients. rSO 2 decreased to a low value of 53 ± 11% at the end of DHCA. There was an incremental decrease in the rSO 2 during the period of DHCA. The values from the start of DHCA to 40 min at 5-min increments were 88 ± 7%, 79 ± 9%, 75 ± 9%, 67 ± 10%, 64 ± 11%, 60 ± 11%, 56 ± 12%, and 53 ± 8%. The greatest decrease in the rSO 2 value occurred during the initial 5 min of circulatory arrest (9 ± 3%). Over the entire time of DHCA, there was an average decrease in the rSO 2 value of 0.9% per minute (range: 0.5 to 1.6% decrease per minute). Of the 8 patients, only one developed a post-operative problem with mild developmental delay and spastic diplegia. With physical therapy and early childhood intervention, he continues to improve. The nadir of the rSO 2 values in this patient were 43% and 45% and the maximal rSO 2 achieved prior to the onset of DHCA was 87% and 74%.


   Discussion Top


The current cohort of patients provides preliminary data regarding the performance of the NIRS monitor during DHCA. We noted an incremental decline in the rSO 2 during DHCA with an average decrease of 0.9% per minute. The decline was greatest during the first 5 min and then stabilised out over the remainder of the DHCA time. Also, it was noted that despite the conventional thinking that 15 min of cooling on CPB is adequate prior to the onset of DHCA, 3 of the 8 patients had not achieved a maximal rSO 2 value at that time despite achieving a nasopharyngeal temperature of 17-18°C and burst suppression on the EEG monitor. There was variability in the maximal rSO 2 value that could be achieved during CPB and cooling as the rSO2 values at the end of cooling varied from 74 to 95% in the 8 patients. In one patient who manifested post-operative neurocognitive dysfunction, the nadir rSO 2 value at the completion of DHCA was in the low range of 40% and the maximal rSO 2 value that could be achieved prior to initiating DHCA was only 74%. With the obvious limitation of a small cohort of only 8 patients, it is difficult to make any definitive comment regarding which rSO 2 values are indicative of the potential for post-operative neurocognitive issues; however, it may be that the pre-circulatory arrest value is also important in such outcomes.

The most important issues regarding the use of NIRS monitoring in clinical practice are as follows: first, the rSO 2 value that is predictive of neurological damage, and second, will changes in clinical care based on NIRS values alter the post-operative neurological outcome. To date, there are limited animal or human data on the basis of which these important clinical issues can be answered. Using a neonatal piglet model with exposure to increasing degrees of cerebral hypoxemia, Kurth et al. demonstrated that the threshold for 50% of the animals to demonstrate an increased cerebral lactate concentration was a rSO 2 value of 44%. [8] Fifty percent of the animals manifested minor EEG changes at an rSO 2 value of 42%, major EEG change at an rSO 2 value of 37%, and decreased brain adenosine triphosphate at an rSO 2 of 33%. In a piglet model of DHCA, Sakamoto et al. , compared changes in NIRS and its correlation with the eventual outcomes (neurologic and pathologic) under varying clinical conditions, including haematocrit (20% versus 30%), temperature (15°C versus 25°C), blood gas management (pH-stat versus a-stat), and duration of circulatory arrest (60 to 100 min). [9],[10] The nadir rSO 2 occurred more quickly at a higher temperature, lower haematocrit, and when using a-stat versus pH stat blood gas management. The duration of lowest rSO 2 correlated with eventual neurologic outcome determined by both clinical examination and histologic examination of the neuronal tissue. Ausman and colleagues monitored rSO 2 values during DHCA for aneurismal clipping in 7 adult patients [11] and noted no neurological damage when the rSO 2 values remained above 35%. In the one patient whose values were less than 35%, there was postmortem examination evidence of global cerebral hypoxia.

In an observational study, Kurth et al. used an NIRS and measured what they termed 'the cerebrovascular haemoglobin oxygen saturation' (S CO2 ) in 26 infants and children undergoing cardiac surgery for CHD using CPB and DHCA. [12] They found that the S CO2 increased during cooling and CPB by 30 ± 4% from baseline and then decreased by 62 ± 5% by the end of the DHCA which varied from 17 to 60 min. During DHCA, S CO2 decreased to a nadir which was approximately 60%-70% of baseline values obtained pre-bypass. The nadir was reached at 20-40 min of DHCA, after which there was no further decrease. They speculated that this point correlates with a time when there is no additional oxygen available for uptake by the brain and that the time required to reach the rSO 2 nadir correlated with clinical and experimental studies suggesting that 45 min is the safe duration for DHCA. [13],[14] The 3 patients who had acute post-operative neurological changes (seizures in 1 and prolonged coma in 2) had a smaller increase in rSO 2 after the onset of CPB (3% versus 33% in patients without neurological deficit) and the duration of cooling before DHCA was shorter.

The data from the current cohort of patients provides preliminary data regarding the performance of a commercially available NIRS monitor. In our experience, we noted that there is a predictable decrease in rSO 2 values during DHCA of approximately 0.9% per minute. The decrease was greater during the initial 5 min of DHCA and then stabilised thereafter at approximately 0.9% per minute. Clinical and follow-up data have suggested that the incidence of neurocognitive complications related to DHCA increases after 40 min. [2] This incidence is no different in patients with DHCA of duration of less than 40 min when compared with patients undergoing cardiac surgical procedures without DHCA. [2] Although the absolute value of rSO 2 at which neurological damage occurs remains undetermined, the clinical and animal data would suggest a value of approximately 40%-45%. Given a starting value of 90% and a decrease of 1% per minute, our data would suggest that it would take approximately 40 min to reach an rSO 2 value of 45%. Therefore, the NIRS data from the current cohort is line with the clinical data suggesting a safe duration of DHCA of 40 min. However, our data shows that there is a significant interpatient variability as the rSO 2 decline varied from 0.5 to 1.6% in the 8 patients. We could identify no clinical variable (temperature, haemoglobin, age or starting rSO 2 value) responsible for this variability.

Given that one of the many risk factors for neurological damage is the duration of low rSO 2 values, it would be logical to maximise rSO 2 values prior to instituting DHCA to limit the duration of low rSO 2 values. Our data also suggests that NIRS monitoring is useful in ensuring a maximum rSO 2 value prior to the onset of DHCA. In our cohort of 8 patients, there were 3 patients who required CPB and cooling for longer than 15 min, despite achieving a nasopharyngeal temperature of 17-18°C and a burst suppression pattern on the EEG monitor. We also noted that there was one patient in whom the maximum rSO 2 value was only 74%. If the inability to achieve a high rSO 2 is in fact a risk factor for neurocognitive damage, we would speculate that options to consider in such patients may include intermittent periods of brief low-flow cardiopulmonary bypass or more profound degrees of hypothermia. [15],[16]

There are several limitations of the current study, most importantly the cohort size of only 8; however, given the decreasing use of DHCA, the collection of a large enough group may not be feasible from a single institution. Additionally, the authors do not have a control group in whom rSO 2 was not monitored. Given that rSO 2 monitoring is now standard of care for their practice, they do not feel that they can ethically have a control group in whom rSO 2 is not monitored. Despite the limited number of patients, the NIRS changes during DHCA were reproducible between the patients and these data demonstrate that despite 15 min of cooling on CPB, a subset of patients may not achieve a maximum rSO 2 value. However, there are important questions which remain unanswered. They are, lack of demonstration of an outcome benefit if the rSO2 is maximised prior to DHCA and lack of explanation of the fact that some patients cannot achieve a sufficiently high rSO 2 despite cooling on CPB.

 
   References Top

1.Freed DH, Robertson CM, Sauve RS, Joffe AR, Rebeyka IM, Ross DB, et al . Intermediate-term outcomes of the arterial switch operation for transposition of the great arteries: Alive but well? J J Thorac Cardiovasc Surg 2006;132:845-52.  Back to cited text no. 1    
2.Gaynor JW, Nicolson SC, Jarvik GP, Wernovsky G, Montenegro LM, Burnham NB, et al . Increasing duration of deep hypothermic circulatory arrest is associated with an increased incidence of postoperative electroencephalographic seizures. J Thorac Cardiovasc Surg 2005;130:1278-86.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.Ferry PC. Neurologic sequelae of open-heart surgery in children: An "irritating question.". Am J Dis Child 1990;144:369-73.  Back to cited text no. 3    
4.Greeley WJ, Kern FH, Meliones JM, Ungerleider RM. Effect of deep hypothermia and circulatory arrest on cerebral blood flow and metabolism. Ann Thor Surg 1993;56:1464-6.  Back to cited text no. 4    
5.Wypij D, Newburger JW, Rappaport LA, duPlessis AJ, Jonas RA, Wernovsky G, et al . The effect of duration of deep hypothermic circulatory arrest in infant heart surgery on late neurodevelopment: The Boston circulatory arrest trial. J Thor Cardiovasc Surg 2003;126:1397-403.  Back to cited text no. 5    
6.Jobsis FF. Noninvasive, infrared monitoring of cerebral and myocardial oxygen sufficiency and circulatory parameters. Science 1977;198:1264-7.  Back to cited text no. 6    
7.Tobias JD. Cerebral oxygenation monitoring: Near-infrared spectroscopy. Expert Rev Med Dev 2006;3:235-43.  Back to cited text no. 7    
8.Kurth CD, Levy WJ, McCann J. Near-infrared spectroscopy cerebral oxygen saturation thresholds for hypoxia-ischemia in piglets. J Cereb Blood Flow Metab 2002;22:335-41.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Sakamoto T, Zurakowski D, Duebener LF, Hatsuoka S, Lidov HG, Holmes GL, et al . Combination of alpha-stat strategy and hemodilution exacerbates neurologic injury in a survival piglet model with deep hypothermic circulatory arrest. Ann Thorac Surg 2002;73:180-9.   Back to cited text no. 9  [PUBMED]  
10.Sakamoto T, Hatsuoka S, Stock UA, Duebener LF, Lidov HG, Holmes GL, et al . Prediction of safe duration of hypothermic circulatory arrest by near-infrared spectroscopy. J Thorac Cardiovasc Surg 2001;122:339-50.   Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Ausman JI, McCormick PW, Stewart M, Lewis G, Dujovny M, Balakrishnan G, et al . Cerebral oxygen metabolism during hypothermic circulatory arrest in humans. J Neurosurg 1993;79:810-5.  Back to cited text no. 11  [PUBMED]  
12.Kurth CD, Steven JM, Nicolson SC. Cerebral oxygenation during pediatric cardiac surgery using deep hypothermic circulatory arrest. Anesthesiology 1995;82:74-82.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]
13.Newburger JW, Jonas RA, Wernovsky G, Wypij D, Hickey PR, Kuban KC, et al . A comparison of the perioperative neurologic effects of hypothermic circulatory arrest versus low-flow cardiopulmonary bypass in infant heart surgery. N Engl J Med 1993;329:1057-64.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]
14.Bellinger DC, Jonas RA, Rappaport LA, Wypij D, Wernovsky G, Kuban KC, et al . Developmental and neurologic status of children after heart surgery with hypothermic circulatory arrest or low-flow cardiopulmonary bypass. N Engl J Med 1995;332:549-55.  Back to cited text no. 14  [PUBMED]  [FULLTEXT]
15.Gillinov AM, Redmond JM, Zehr KJ, Troncoso JC, Arroyo S, Lesser RP, et al . Superior cerebral protection with profound hypothermia during circulatory arrest. Ann Thor Surg 1993;55:1432-9.  Back to cited text no. 15    
16.Schultz S, Antoni D, Shears G, Markowitz S, Pastuszko P, Greeley W, et al . Brain oxygen metabolism during circulatory arrest with intermittent brief periods of low-flow cardiopulmonary bypass in newborn piglets. J Thor Cardiovasc Surg 2006;132:839-44.  Back to cited text no. 16    

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Correspondence Address:
Joseph D Tobias
Department of Anesthesiology Chief, Division of Pediatric Anesthesiology, Russell and Mary Shelden Chair in Pediatric Intensive Care Medicine. Professor of Anesthesiology and Child Health, University of Missouri, Department of Anesthesiology, 3W40H, One Hospital Drive, Columbia, Missouri - 652 12
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.43057

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