NEUROPROTECTIVE CARE IN ACTION:

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1 NEUROPROTECTIVE CARE IN ACTION: aeeg & NIRS monitoring No Disclosures or Conflicts of Interest Alexis Davis, MD, MS Epi Care of the Newborn Brain Symposium September 14, 2017 Overview aeeg Understanding the technology Basics of aeeg Interpretation Strip review NIRS Understanding the technology Clinical applications and case studies Troubleshooting and interventions Objectives aeeg Understand the basis for and limitations of aeeg monitoring Recognize the 5 background patterns for aeeg and their classification as normal vs. abnormal NIRS Identify two applications for NIRS monitoring Describe two strategies to respond to low cerebral oxygen saturations 1

2 aeeg History of aeeg 1960s: development for use in monitoring depth of anesthesia 1980s: initial application of aeeg to term newborns with HIE 2000s: expansion to preterms, metabolic disorders Now: standard monitoring during therapeutic hypothermia (aong with ceeg) Summary of the aeeg technology 3-channel bedside aeeg for brain activity and seizure detection How does EEG become aeeg? ANALOG / DIGITAL CONVERTER SENSORS DAU MONITOR slide courtesy of K. Randall, BrainZ Toet et al, Clin Perinatol 2008; 35:

3 Peak-to-peak amplitudes: upper and lower borders of the aeeg aeeg Lead Placement Five hydrogel electrodes 4 scalp electrodes: C3, C4, P3, P4 1 reference/ground electrode (usually on the back) 3 channels for monitoring: P3-P4: traditional channel to monitor zone most at risk for ischemia in infants with HIE C3-P3 C4-P4 Use to compare brain activity between hemispheres I. Rosén Clin Perinatol 2006; 33: aeeg Interpretation The 7 S s of systematic review 1. Story/situation 2. Signal quality 3. Strength of brain activity 4. Sleep wake cycles (SWC) 5. Symmetry 6. Suspicious areas (seizures, artifacts) 7. Stability or Changes in the Background Pattern 3

4 1. Story/situation Why are you monitoring the baby? Gestational/corrected age Neurologic exam Medications 2. Signal quality aeeg devices have sensors to assess the signal quality poor signal quality can lead to artifacts in the aeeg tracing Goal impedance? In other words, do you expect the aeeg to be normal or abnormal? 3. Strength of activity: Background pattern classification Continuous normal voltage Discontinuous Lower margin > 5 μv Upper margin μv Lower margin < 5 μv Upper margin > 10 μv Normal +/- Normal Normal trace: Continuous voltage (CNV) Burst suppression Continuous low voltage Isoelectric/flat tracing Lower margin <2 μv Bursts > 25 μv Lower margin < 5 μv Upper margin < 10 μv Lower margin 0-1 μv Upper margin < 5μV Abnormal Abnormal Abnormal Lower margin > 5µV Upper margin > 10µV Neoreviews 2006; 7: e76-e87 4

5 Discontinuous background Continuous/Discontinuous voltage; immature SWC Lower margin < 5µV Upper margin > 10µV Neoreviews 2006; 7: e76-e87 Neoreviews 2006; 7: e76-e87 Burst Suppression (BS) patterns BS+ BS- Continuous low voltage Lower margin < 2 µv, flat Upper margin > 10µV due to bursts Neoreviews 2006; 7: e76-e87 Lower margin < 5µV Upper margin < 10µV Neoreviews 2006; 7: e76-e87 5

6 8/14/17 4. Sleep Wake cycles Isoelectric/flat Mature SWC * * * Immature SWC Lower margin < 5µV (usually 0-1µV) Upper margin < 5µV Kuhle et al, Wien Klin Wochenschr 2001; 113: Neoreviews 2006; 7: e76-e87 Sleep-wake cycles Definitions for mature vs. immature SWCs Sommers R et al Ped Res 2013; 74(6): Mature cycle: duration of 20-60min upper border voltage increase by at least 10% vs. preceding or subsequent 20min of recording lower border voltage decrease to at least 5mV for 50% of cycle duration, or at least 15% lower than the preceding or subsequent 20min of recording Immature cycle: 20-60min with lower border voltage meeting mature criteria min with upper and lower border voltages for mature criteria Interrupted cycle: Fulfills mature criteria but is <20 min El-Dib, Pediatr International

7 8/14/17 5. Symmetry Mature (using 2 channel view) R Immature L R L Interrupted Figure 4 Ross Sommers (2013) 74, doi: /pr Suspicious areas/seizures 7. Stability or Changes in the Background Pattern Term infant, STAT C/Sect, APGARs 11, 45 & 410 3hrs of age Cooled in ICE study 7

8 Challenge: differentiating signal from artifact HFOV artifact EKG artifact EMG artifact 8

9 Pitfalls/caveats of aeeg interpretation Pitfalls/artifacts in seizure detection 5µV Patting/burping Respiratory/EKG How to differentiate artifact from seizures Look for build-up vs. regularity Manipulate x- and y-axis, inspect absolute voltages and frequencies of suspected ictal activity high frequency artifact electrodes repositioned following paralysis *Important to inspect raw EEG, document relevant clinical events in the interpretation of the aeeg* Hagmann, C. F. et al. Pediatrics 2006;118: Copyright 2006 American Academy of Pediatrics STRIP REVIEW 9

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11 Clinical Scenario #1 Baby born at 32 weeks 2 day history of decreased fetal movements Required significant DR resuscitation Initial Hct 15% -> feto-maternal hemorrhage Exam c/w severe encephalopathy* 10 hours of life: DOL3 11

12 DOL5 DOL8 DOL10 SEIZURE EXAMPLES 12

13 8/14/17 Beginning Middle Middle End 13

14 Example: seizure Example: seizure 14

15 Clinical Scenario #2 Infant born at 26 weeks Initially on non-invasive positive pressure support DOL5: clinical decompensation, severe metabolic acidosis, presumed sepsis Head US with evolving encephalomalacia Days later.?clinical seizures -> aeeg placed 15

16 Following phenobarbital load Seizure-single channel view NIRS 16

17 With Permission from Covidien, Inc. What is NIRS? Continuous, real-time, non-invasive bedside monitor of regional tissue oxygenation (rso 2 ) Validated with jugular venous saturations FDA approved for use in infants (including those <2.5 kg) How does NIRS work? From Rais-Bahrami, et al. J Perinatol, (a) Placement of sensor on neonate's forehead with light source and detector. (b) Light passes from light source to detector after passage through scalp, skull, and brain tissue. (c) Tissue oxygen saturation (rso 2 ) reflects a ratio of arterial and venous blood (25%:75%) Why do NIRS monitoring? Standard pulse oximetry may not reflect end-organ oxygenation Why? Cerebral autoregulation Systemic steal (cardiac defects, PDA) NIRS values rso 2 Term (%, D1) Preterm (%) Cerebral 78 ± Renal 92 ± Mesenteric 70 ± McNeill S, J Perinatol, 2011; Verhagen EA, Acta Paediatrica, 2007; Grossauer K, Arch Dis Child Fetal Neonatal Ed, 2009; Bernal NP, J Ped Surg, What is a critical value? -Notify MD if sustained cerebral rso 2 <50% Animal model cellular injury if <40% MRI changes if <40% in cardiac patients 17

18 Who May Benefit from NIRS Monitoring? Preterm infants with hemodynamic instability, impaired auto-regulation, anemia, patent ductus arteriosus Term infants with: Congenital heart disease pre-ecmo/ecmo Hypoxic ischemic encephalopathy Undergoing exchange transfusion ØAny infant where there is concern for inadequate cerebral flow Application of NIRS in the NICU Research tool Understand the effect of clinical management strategies on cerebral oxygenation Guide clinical management Is a PDA clinically significant? Ventilator management Determine need for transfusion When to do cardiac surgery? Application in preterms: PDA NIRS Project PDA NIRS Project: Results Cerebral Saturation after PDA treatment Indomethacin Treatment 1st dose 2nd dose 3rd dose p=0.02 * Surgical Ligation Ductal clip placed Chock VY, et al. Neonatology

19 PDA Autoregulation Cerebral autoregulation Brain maintains constant perfusion pressure despite fluctuations in systemic blood pressure Intact Autoregulation PDA Autoregulation Lack of concordance between MAP and rso2, r=0.43 Impaired cerebral autoregulation Measured as concordance (r>0.5) between mean arterial blood pressure (MAP) and rso 2 (pressure passive cerebral circulation) Common in preterm infants (Soul, et al. Pediatr Res 2007) Associated with mortality, severe IVH/PVL (Tsuji, et al. Pediatrics, 2000) Impaired Autoregulation Concordance between MAP and rso2, r=0.82 Chock VY, et al. J Pediatr, 2012 PDA Autoregulation: Results Average PPI in neonates following surgical PDA ligation is transiently increased for 2h and normalizes by 6h post-op. * *p=0.04 **p<0.001 PDA NIRS Project: Conclusions Infants undergoing surgical ligation had a significant increase in cerebral oxygenation (>20% change from baseline) when compared to conservatively managed or indomethacin-treated patients. Vigilance for cerebral pressure passivity is warranted in infants undergoing surgical PDA ligation, especially in the 6 hours after surgery Strategies to maintain stable cerebral blood flow should be enacted * * Chock VY, et al. J Pediatr,

20 Is a PDA Significant? Example #1: Baby O 24 week preterm infant 18 days of age found to have a large PDA with left to right shunting Cerebral sats 25-45%, Renal sats 15-50% (NOTE: the monitor does not register <15%) Indicator of poor cerebral/systemic perfusion Decision made for PDA ligation Is a PDA Significant? Example #2: 8 day old, 26 week infant with PDA, L to R shunt by ECHO Renal sats much lower than cerebral sats Renal sats with severe variability (15-60%) Decision to give Indocin Renal sats with higher baseline and less variability after treatment Is a PDA Significant? After Tx: Renal sats higher with less variability Before Tx: Renal sats significantly depressed at baseline with extreme variability Is PDA significant? Example #3: 3 week old ex 25 week infant LOUD murmur, large PDA confirmed on echocardiogram Non-invasive positive pressure support Cerebral saturations mostly ~60%, some dips into 50s Renal saturations low, 20-30% Conservative management era: Increase PEEP on ventilator Transfuse prbcs Relative fluid restriction 20

21 Prematurity and IVH Example #4: 25 week preterm infant Intestinal perforation requiring surgery Cerebral sats 55-65, then decreased to low 40 s, Mesenteric sats initially 50 s, then decreased to 30 s Prompted HUS revealing bilateral giii/iv IVH 24-week triplet with bilateral grade 4 IVH and ventriculomegaly. Prolonged periods with Csat <40%. Corresponding aeeg with discontinuous vs burst suppression tracing. PRBC transfusion with transient increase in Csat. Prematurity and Anemia Tissue Oxygenation after PRBC transfusion Prematurity and Anemia Changes in cerebral oxygenation (Csat) do not corrrelate with Hct, but may trend with pre-transfusion Csat Transfusion complete t Chock VY, et al. PAS

22 Prematurity and Anemia Mesenteric Oxygenation in Subjects Developing Feeding Intolerance *p=0.04, **p=0.01 at 15 and 24 hours after completion of transfusion Prematurity and Anemia: Conclusions Cerebral oxygenation increased by 1.5% every hour during PRBC transfusion, and levels were sustained for at least 24 h (p<0.0001). Mesenteric oxygenation increased by 1.2% every hour during PRBC transfusion (p=0.04) and lower levels were associated with feeding intolerance. Changes in Hct may not reflect end-organ oxygenation Role of NIRS during transfusions Chock VY, et al. PAS 2011 Chock VY, et al. PAS 2011 Monitoring infants with CHD High risk for CNS injury pre-operatively Chromosomal anomalies/ brain dysgenesis Acquired hypoxic-ischemic injury Ductal dependent lesions with diastolic run-off compromising brain and other end-organ perfusion Increased risk of emboli after balloon atrial septostomy in TGA patients (McQuillen et al, Circulation, 2006) Ongoing systemic inflammation Altered cerebral autoregulation (esp in preterm infants) What can NIRS tell us in CHD patients? Indirect measure of Qp:Qs Regardless of systemic O 2 sat values, cerebral and somatic oxygenation may be inadequate Cerebral oxygenation Poor end organ perfusion may require interventions to increase systemic blood flow or consider need for earlier surgery Splanchnic oxygenation May provide reassurance for initiation of feeds - or evidence to keep NPO 22

23 Interventions amenable to NIRS monitoring in cardiac patients Ventilator changes Changes in PGE dose Rashkind or valvuloplasty procedures Other mechanisms to improve Qp:Qs Subatmospheric oxygen (nitrogen) Milrinone NIRS use in CHD patients Johnson, et al. Near-Infrared Spectroscopy in Neonates before Palliation of Hypoplastic Left Heart Syndrome Annals of Thorac Surg, 2009 Compared historical cohort of patients with HLHS without NIRS monitoring to a recent cohort that received pre-operative NIRS monitoring of cerebral and somatic tissue saturations Routine use of NIRS monitoring resulted in reduced use of mechanical ventilation, reduced use of inspired nitrogen, and no impact on mortality or length of hospital stay NIRS use in CHD patients Example #5: Term infant with TGA Systemic SpO2 stable s Cerebral Csat 50% with dips to low 30%, Renal sats 45-55% Concern for inadequate cerebral blood flow Decision made to go to OR sooner than originally planned NIRS and Pre-ECMO patients PPHN/Meconium aspiration Optimize both systemic oxygenation AND cerebral oxygenation Effect of hypocarbia 23

24 NIRS and Hypoxic-ischemic encephalopathy Trouble-shooting NIRS Use Still being studied Small studies suggest that infants with adverse neurodevelopmental outcomes after cooling for HIE have unusually high rso 2 in the first 24h (80±9% vs 67±8%) Meek, et al. Arch Dis Child Fetal Neonatal Ed, Toet, et al. Pediatrics High Csat represents a failure of O 2 extraction Ancora, et al. Brain Dev. Jan 2013 What to do if not picking up a reading? Check sensor adherence Check connections Too much ambient light? (e.g. phototherapy) Skin integrity-- esp in preemies Check sensor site every 24 h and change sensor at least every 4 days Avoid direct pressure over sensor Use Mepitel barrier between skin and sensor Slow and gentle removal Potential interventions for low NIRS values What to do with low values? Is infant hypotensive? Is infant anemic? Is infant hypocarbic (poor cerebral perfusion)? Is infant hypoxic? Consider reducing cerebral metabolic rate (sedation, control hyperthermia) For cardiac patients: Do values correlate with other indicators of poor systemic perfusion (i.e. high lactate levels, prolonged CR, cold extremities, low UOP) Consider interventions to improve Qp:Qs (I.e. PEEP, subatmospheric oxygen, milrinone, transfusion to increase Hct, change in PGE dosing, earlier surgical intervention) Challenges/limitations of NIRS Absence of clear normative values in large populations Different devices use different opitcal probes and algorithms Wide inter-patient variability Important to establish baseline in each patient 24

25 Which monitoring? And who? Diagnosis Duration (d) Monitor type HIE/Cooling 4+ aeeg/ceeg & NIRS Seizures 3+ aeeg/ceeg ECMO/pre-ECMO 7 aeeg (ceeg), NIRS Grade 3/4 IVH or hydrocephalus 7+ aeeg (ceeg) Preemie <= 29 weeks 7 NIRS CNS anomalies 7 aeeg (ceeg) Metabolic disease 7 aeeg (ceeg) Cyanotic CHD 7 NIRS Meningitis 7 aeeg (ceeg) Symptomatic PDA 7 NIRS ALTE/BRUE 3 aeeg/ceeg Severe jaundice 3 NIRS, consider aeeg 25