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Keeping a “COOL” Head Lina Chalak, MD Updates on Neonatal Asphyxia

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Presentation on theme: "Keeping a “COOL” Head Lina Chalak, MD Updates on Neonatal Asphyxia"— Presentation transcript:

1 Keeping a “COOL” Head Lina Chalak, MD Updates on Neonatal Asphyxia
Assistant Professor Division of Neonatology, Pediatrics University of Arkansas Medical Center

2 Outline Importance of Pathogenesis/ Definitions
Early Identification of High risk NBN New Treatment strategies: Cooling.

3 Pathogenesis Impaired cerebral blood flow is the principal mechanism leading to perinatal brain injury It occurs as a consequence of interruption of placental blood flow and gas exchange

4 Neuropathology- Importance of Cerebral Blood Flow

5 Definitions Hypoxia - refers to an abnormal reduction in oxygen delivery to the tissue Ischemia - refers to a reduction in blood flow to the tissue Asphyxia - refers to progressive hypoxia, hypercarbia and acidosis. Severe Fetal Acidemia: Cord arterial pH < 7.00

6 Hypoxic-Ischemic Encephalopathy
A sentinel perinatal event at Delivery + Apgar Score < 3 at 5 min + Cord pH < 7.00 + Encephalopathy by exam (stage 2-3) + Evidence of Non CNS dysfunction

7 Fact Although interference in placental blood flow and consequently gas exchange is fairly common, residual neurologic sequelae are infrequent and are more likely to occur when the asphyxial event is severe.

8 Why? The fetus immediately adapts to an asphyxial event to preserve cerebral blood flow and oxygen delivery

9 CARDIOVASCULAR RESPONSES TO ASPHYXIA
ASPHYXIA (PaO2, PaCO2, pH) Redistribution of Cardiac Output Cerebral, Coronary, Adrenal Renal, Intestinal Blood Flow Blood Flow Ongoing Asphyxia Cardiac Output Cerebral Blood Flow

10 Early Identification of High Risk Infants Requires a Combination of Factors
1) Evidence of an Acute Perinatal Insult Indicated by a combination of markers* 1) Sentinel event 2) Delivery room resuscitation 3) 5 Minute Apgar score  5 4) Cord arterial pH  7.00 + 2) Postnatal evidence of encephalopathy 1) Clinical 2) EEG

11 Clinical: Assessment of Encephalopathy
Neurologic Evaluation Level of Consciousness Neuromuscular control Reflexes Autonomic function Evidence of Seizures Staging of Encephalopathy Stage 1 - Mild Stage 2 - Moderate Stage3 - Severe Sarnat Arch of Neurol. 33;696,1976

12 Long term outcome of term infants with HIE
Death Disability Mild Moderate % % Severe 60% %

13 Fact The ability to identify EARLY on, infants at highest risk for HIE is critical : The therapeutic window for intervention strategies to be effective in preventing the processes of ongoing injury in the newborn brain is short (< 6 hours) Novel therapeutic strategies to prevent ongoing injury have the potential for significant side effects

14 a-EEG: Assessment of Cerebral Function
A Cerebral Function Monitor via a single channel EEG (a-EEG), records activity from biparietal electrodes. The signal is smoothed and the amplitude integrated. Naqeeb, et al. Pediatrics 1999:103:1263

15 Representative aEEG tracings
Normal Low line tracing above 5 cuttoff High line above 10 cuttoff Moderately Suppressed Low line below 5 cutoff High line above 10 cutoff Severely Suppressed Low line below 5 cutoff High line above 10 cutoff

16 50 infants with an acute perinatal insult
Clinical examination/Sarnat stage 2 or 3 a-EEG assessment/ Mod or severe Outcome: Persistent encephalopathy > 5 days Occurred in 14/50 infants Abnormalities in both the Clinical and a-EEG evaluation enhances the early detection of infants who progress to irreversible brain injury.

17 Management Beyond the Delivery Room
General Measures Neuroprotective Strategies

18 inhibitors POTENTIAL STRATEGIES FOR PREVENTING REPERFUSION INJURY
HYPOXIA-ISCHEMIA ANAEROBIC GLYCOGLYSIS MILD HYPOTHERMIA ATP ADENOSINE GLUTAMATE NMDA RECEPTOR BLOCKER MAGNESIUM SULFATE DEXTROMETHORPHAN KETAMINE NMDA RECEPTOR HYPOXANTHINE Ca++ XANTHINE OXIDASE INHIBITORS NOS INHIBITORS ALLOPURINOL LIPASES XANTHINE ARACHIDONIC ACID NITRIC OXIDE SYNTHASE inhibitors FREE RADICAL SCAVENGERS SUPEROXIDE DISMUTASE LAZEROIDS FREE RADICALS EICOSANOIDS

19 mediating neuronal death following ischemia are temperture dependent.
A COOL HEAD !!!! Recent evidence indicates that mechanisms mediating neuronal death following ischemia are temperture dependent. Mild to modest decreases in brain temperature may greatly influence the resistance of the Brain to brief periods of ischemia.

20 Potential Mechanisms of Action of Hypothermia
Reduces cerebral metabolism Preserves ATP levels Decreases energy utilization Suppresses Excitotoxic AA accumulation Reduces NO synthase activity Suppresses free radical activity Inhibits apoptosis Prolongs therapeutic window?

21 Potential Adverse Effects of Hypothermia in Neonates
Hypertension Cardiac arrhythmia Persistent acidosis Increased oxygen consumption Increased blood viscosity Reduction in platelet count Pulmonary hemorrhage Sepsis Necrotizing enterocolitis

22 COOLING METHODS COOLING CAP COOLING BLANKET

23 Available therapies in 2005
Brain cooling vs. Total body cooling - Must be initiated within 6 hrs after birth - Duration of cooling is 72 hours - Extent of cooling is 33 degrees celcius.

24 Lancet. 2005;365:

25 Selective Head Cooling
July , 25 centers UK/US 234 term infants with encephalopathy and abnormal Aeeg Randomized by 6 hours after birth Control vs. cooling cap for 72 hours Goal rectal temperature c Primary outcome death or severe disability by 18 months

26 N Engl J Med 2005;353:

27 Whole Body Cooling Trial
208 infants > 36 weeks gestation with HIE (Moderate to severe encephalopathy) Enrolled within 6 hours after birth in a randomized controlled trial Control vs. whole body cooling with goal esophageal temperature of 33.5 c for 72 hours Follow up months Main outcome death or moderate or severe disability (BAYLEY, HEARING, BLINDNESS)

28 Primary Outcomes in 2 Trials
Control Cool OR p Cool cap 66% % Whole body62% %

29 Secondary Outcomes for 2 Trials
Control Cool P Cool cap % % -Mod EEG % % -Severe EEG % % Whole body % % -Sarnat % % -Sarnat % %

30 Keeping a cool head …. Thank you


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