TLC March 27, Shawn Hollinger-Neonatal Fellow CHEO

Transcription

1 TLC March 27, 2013 Presented/Prepared by: Shawn Hollinger, PGY5 Neonatal-Perinatal Medicine Resident - University of Ottawa With slides/images from Dr. Brigitte Lemyre Associate Professor of Pediatrics University of Ottawa 1. Define Neonatal Encephalopathy and Perinatal Asphyxia and identify infants at risk 2. Outline the types of neonates that may benefit from therapeutic hypothermia 3. Review the risks and benefits of therapeutic hypothermia in neonates with perinatal encephalopathy 4. Discuss some practical issues that may be important for referring centers Neonatal Encephalopathy Clinically defined as a syndrome of deranged neurological function in the earliest days of life in the term infant, manifested by difficulty with initiating and maintaining respiration, depression of tone and reflexes, subrmal level of consciousness and often by seizures devries et al. Newborn Brain Symposium 2008 Perinatal Asphyxia ACOG all of the following required profound metabolic or mixed acidemia umbilical artery ph < 7.00 persistent Apgar score of 0-3 for 5 or more minutes evidence of neonatal neurologic sequelae (seizures, coma, hypotonia) one or more of cardiovascular, gastrointestinal, hematologic, pulmonary or renal system dysfunction CHEO 23% of 4 million annual global neonatal deaths are caused by asphyxia Incidence of moderate to severe birth asphyxia in developed countries 1-2/ % of infants die or suffer severe handicap 1

2 Conditions That Predispose the Fetus and Newborn Infant to Asphyxia Maternal Prepartum Intrapartum Neonatal Obstetric Initial injury Reperfusion Secondary injury Toxemia (eclampsia) Abruptio Placentae Abrmal Presentation Prematurity Diabetes Mellitus Prolapse of Umbilical cord Precipitate delivery Respiratory Distress Drug addiction Placenta previa Prolonged labour Cardiopulmonary amalies Cardiovascular Disease Hydramnios Difficult forceps delivery Infectious disease Premature rupture of fetal membranes Intrauterine growth retardation Infectious disease Hemolytic disease Isoimmunization Multiple pregnancy Prolonged pregnancy Septic or viremic shock Primary damage Vulnerable area Neurological Signs Seizures Abrmal Respiratory Pattern Hyperalertness, Obtundation or Coma Jitteriness Posturing Impaired suck, swallow or gag Abrmal pupillary responses Abrmal tone Lungs: PPHN, surfactant disruption, MAS Kidneys: oliguria, ATN Heart: Tricuspid regurgitation, myocardial necrosis, shock Metabolic: acidosis, hypoglycemia/na/ca GI: NEC, hepatic dysfunction Hematology: DIC, thrombocytopenia Adrenal insufficiency Acidosis Lactate Hypoglycemia Coagulopathy Increased Urea & Creatinine (often later) Increased AST, ALT & GGT (often later) Other signs depending on the cause Sarnat and Sarnat Arch Neurology infants > 36 wks, fetal distress or Apgar 5 or less at 1 or 5 minutes serial neurologic exams and EEGs in hospital and at follow-up defined rmal as within 1 month of 50th percentile on Denver, absence of hemiparesis or focal neurologic deficits, rmal muscle tone and reflexes and rmal EEG

3 Hyperalert Normal tome, overactive reflexes Strong Moro, rmal or weak suck Generalized sympathetic function increased: mydriasis, tachycardia No seizures, rmal EEG Lethargic or obtunded Hypotonic Weak or absent suck, weak Moro Generalized parasympathetic function increase: miosis, bradycardia Common seizures, abrmal EEG Stuporous Flaccid, intermittent decerebrate posturing Absent suck, gag, Moro Depressed automic function: variable pupils, variable heart rate Very abrmal EEG: burst suppression, isoelectric Supportive Homeostasis Therapeutic Hypothermia Ensure physiologic, oxygen and acid-base balance (Aim for rmal pco2) Correct caloric, fluid and electrolytes disturbances Maintain blood volume and homeostasis Treat infection Monitor for hyperbilirubinemia Treat seizures Klinger G. Arch Dis Child Fetal Neonatal Ed 2005

4 TLC March 27, 2013 Lowers the metabolic rate Essentially resting the brain Decreases the seizure threshold Primary damage Vulnerable area Author/ study Year # of patients Method of cooling aeeg Withdraw reported Follow up Gunn head 18 mo Gluckman head 18 mo Shankaran mo Azzopardi mo Simbruner* Simbruner* mo Zhou head 18 mo Jacobs* months Total number of infants enrolled: 1214 * Stopped early due to lack of clinical equipoise Pooled risk ratio favors therapy RR 0.76 ( ); NNT 7 (5-10) Tagin et al Arch Pediatr Adoles Med 2012 RR 0.67 ( ) NNT 6 RR 0.83 ( )NNT 7 CHEO 1

5 University of Ottawa Criteria: Cord ph <7.0 or base deficit > 16 OR Cord (or baby gas within an hour of birth) ph or base deficit 10 to 15.9 AND History of acute perinatal event (cord prolapse, placental abruption, etc) AND Apgar <6 at 10 minutes or at least 10 minutes PPV Evidence of moderate to severe encephalopathy Clinical seizures OR At least one sign in 3 or more categories on physical exam Category 1. Level of consciousness 2. Spontaneous activity Moderate Encephalopathy Lethargic Decreased activity 3. Posture Distal flexion, full extension 4. Tone Hypotonia (focal, general) 5. Primitive reflexes Suck Moro Weak Incomplete 6. Automic Constricted system Bradycardia Pupils Periodic breathing Heart rate Respirations Severe Encephalopathy Stupor/coma No activity Decerebrate (arms extended and internally rotated, legs extended with feet in forced plantar flexion) Flaccid Absent Absent Skew deviation/dilated/n- reactive to light Variable HR Apnea Presence of kwn chromosomal amaly Presence of major congenital amalies Severe intrauterine growth restriction (weight <2000g) Infants in severe condition for which additional intensive therapy will be offered after discussion with parents by attending neonatologist (i.e. refractory hypotension, refractory acidosis, comatose with absent brain-stem reflexes etc.) Congenital a-rectal amaly based on visual inspection Evidence of head trauma or intracranial hemorrhage Initiated in October 2009 Whole cooling using Blanketroll 3 Aim for C rectal x 72 hours Rewarming over 12h aeeg for neuro monitoring Passive cooling prior to admission aeeg can be used as adjunct in borderline cases Clear biochemical criteria Unclear physical and neuro exam (or evolving) Sarkar J Perinatol 2008

6 Bradycardia ( bpm) Leukopenia (WBC < 5 x 10 9/L) Coagulopathy Hypoglycemia Hypokalemia Shivering Seizures if rewarmed too fast 38 term AGA infants with HIE EEG within 48 hours and neuro f/u > 1 year rmal EEG n=14 rmal outcome (13), mir sequelae (1) extremely abrmal EEG n=10 death (5), major sequelae (4), rmal (1) intermediate EEG n=14 improved background < 7 days good (4/5) progsis Selton and Andre, Neuropediatrics 1997 aeeg is intended to be used clinically to complement the neurologic exam, conventional EEG and neuroimaging aeeg within first 6 hours of life predictive of outcomes at 24 months (n-cooled) Speed of recovery and severity of the abrmality of aeeg is progstically valuable Shah DK et al. Pediatrics 2008 MRI is routinely done on day 4-7 of life Routine MRI images may show signs of significant damages DWI may pick up damage that does t show on the routine imaging Look for damage particularily in the watershed areas and basal ganglia system Volpe JJ. 2001

7 Think about the diagsis! (remember the time-window) When in doubt call transport team to discuss potential candidate Discuss with transport team initiating passive cooling Qualify for the Neonatal Follow Up Clinic (NNFU) Followed at key developmental ages Multidisciplinary team that can identify areas of developmental concern and refer to appropriate services If severe/seizures, may also follow up with neurology Recognize the children that are at risk Advocate that they attend their follow up appointments Utilize developmental tools Follow growth curves including weight and head circumference Possible other therapies/adjuncts Many risk factors for Neonatal encephalopathy If you think a baby might benefit from therapeutic hypothermia, call your referral center to discuss (without delay!) Hypothermia has some side effects, but is effective in cases of moderate to severe encephalopathy Follow up in the community and early recognition of developmental concerns is important Volpe JJ. Neurology of the newborn. De Vries L et al. Long term outcomes after HIE. Arch Dis Child Fetal Neonat Ed 2010;95:F220 Perlman M. HIE prediction of outcome. J Pediatr 2011;158:e51