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NICU Mortality. Objectives. Emphasize the importance of a dequate communication between medical teams, regular and proper evaluation of adequacy of resuscitation Present the Therapeutic Hypothermia Protocol according to the Journal of Clinical Neonatology. R.V. Term B aby Boy NSD
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Objectives • Emphasize the importance of adequate communication between medical teams, regular and proper evaluation of adequacy of resuscitation • Present the Therapeutic Hypothermia Protocol according to the Journal of Clinical Neonatology
R.V. • Term Baby Boy • NSD • 35 y.o. G2P2 (2002) • 39 3/7 weeks AOG • Anthropometrics: • BW 3120g, BL 53cm, HC 34cm, CC 31cm, AC 30cm • AGA • Apgar score: 0, 0, 1, 1, 1
Maternal History • Regular prenatal check-up • Regular intake of multivitamins • Ultrasound – unremarkable • Congenital anomaly scan – normal • Normal OGCT • No BP elevations • CBC and UA upon admission – normal
Past Medical History • No hypertension, no DM Personal/Social History • Occasional alcoholic beverage drinker, nonsmoker, no use of illicit drugs Family History • (+) hypertension, DM, heart disease, colon CA
OB History • G1 – 2009 – NSD, full term male, no fetomaternal complications • G2 – present pregnancy
Admitting CTG: 3hrs 30mins prior to delivery Baseline 130 - 135bpm, with accelerations, no decelerations, good fetal movement, strong contractions every 8 mins
After CEA: 3hrs prior to delivery Baseline 140 bpm, with accelerations, no decelerations, good fetal movement, strong contractions every 8 mins
After AROM: 2hrs 30mins prior to delivery Baseline 135 to 140 bpm, moderate variability, with accelerations, with variable decelerations as low as 60 bpm with slowrecovery, with moderate to strong uterine contractions every 3-4 minutes
1hr and 30mins prior to delivery Baseline 135 to 140 bpm, moderate variability, with accelerations, with variable decelerations as low as 70 bpm with slowrecovery, with moderate to strong uterine contractions every 2-3 minutes
Prior to transfer to DR: 1hr prior to delivery Baseline 130-135 bpm, moderate variability, no accelerations, with variable decelerations as low as 60 bpm with slowrecovery, with moderate to strong uterine contractions every 3-4 minutes
FHT tracing at DR (supine) Change in baseline 120 bpm, moderate variability, no accelerations, with variable decelerations as low as 50 bpm with slowrecovery
Tracing at DR (Left lateral decub): 40mins prior to delivery Maternal heart tone
APGAR Score 39 2/7 0 0 0 0 0 0 0 1 1 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 0 0 1 1
At the NICU • Pale, unresponsive • BP not appreciated, HR 180, on bag-tube ventilation,T 34C • No dysmorphic features • Pupils 8-9mm dilated, not reactive to light • No spontaneous breathing, Equal chest rise, good air entry both lungs • Regular cardiac rhythm, no murmur appreciated • Soft abdomen • Poor pulses, CRT prolonged
Severe Hypoxic-Ischemic Encephalopathy, post cardiopulmonary arrest Initial assessment
Problems • Asphyxia • Mixed Metabolic and Respiratory Acidosis, Intractable Hooked to MV Correction with NaHCO3 Therapeutic Hypothermia
Problems • Shock probcardiogenic • Severe anemia prob sec to hemorrhage PNSS 20mL/kg bolus 2x Dopamine and Dobutamine Drip Blood transfusion ordered but refused
Problems • Infection Ampicillin 50mg/kg/dose Gentamicin 4mg/kg/day
Final Diagnosis Intractable metabolic acidosis secondary to multiorgan dysfunction secondary to perinatal asphyxia
Learning Points • Adequate communication between teams • Regular and proper evaluation of adequacy of resuscitation
Perinatal Asphyxia • Condition of impaired gas exchange that leads to fetal hypoxemia and hypercarbia • Occurs during the 1st and 2nd stage of labor • In term infants, 90% occur in antepartum or intrapartum period as a result of impaired gas exchange across the pacenta • Postpartum – secondary to pulmonary, cardiovascular, neurologic abnormalities Cloherty J. Manual of Neonatal care, 6thed
Hypoxic-Ischemic Encephalopathy • Abnormal neurobehavioral state in which the predominant pathogenic mechanism is impaired cerebral blood flow • Suspected if: • AS <=3 at >5minutes • FHR <60 bpm • Prolonged (>1hr) acidosis • Seizures within the first 24-48hrs after birth • Burst-suppression patten EEG • 20-30% of infants die in the neonatal period Cloherty J. Manual of Neonatal care, Lippincott Williams and Wilkins, 6th ed. 2008 p89 Kliegman R. et al. Nelson Textbook of Pediatrics, 19th Ed. 2011 p571
Sarnat and Sarnat Staging for HIE Kliegman R. et al. Nelson Textbook of Pediatrics, 19th Ed. 2011 p571
Diagnostic Imaging • Diffusion-weighted MRI Kliegman R. et al. Nelson Textbook of Pediatrics, 19th Ed. 2011 p571
Treatment • Therapeutic hypothermia • decreases the rate of apoptosis and suppresses production of mediators known to be neurotoxic, including extracellular glutamate, free radicals, nitric oxide, and lactate. Kliegman R. et al. Nelson Textbook of Pediatrics, 19th Ed. 2011 p571
Therapeutic Hypothermia • >= 36 weeks AOG • Physiological criteria • Evidence of intrapartum hypoxia, including at least two of the following: • 1.Apgar score 5 or less at 10 min • 2. Needing mechanical ventilation and/or ongoingresuscitation at 10 min • 3. Metabolic or mixed acidosis defined as arterial cord gas, or any blood gas within the first hour of life showing pH of 7 or less, or base deficit of ≥12 mmol/l Mosalli R. Whole body cooling for infants with hypoxic-ischemic encephalopathy. J ClinNeonatol 2012;1:101-6.
Therapeutic Hypothermia • Neurological criteria • One of the following: • Seizures is an automatic inclusion • Evidence of encephalopathy suggested a-EEG • Physical examination consistent with moderate to severe encephalopathy Mosalli R. Whole body cooling for infants with hypoxic-ischemic encephalopathy. J ClinNeonatol 2012;1:101-6.
Mosalli R. Whole body cooling for infants with hypoxic-ischemic encephalopathy. J ClinNeonatol 2012;1:101-6.
Infants not Eligible for Cooling • Birth weight less than 2000 g • Gestational age less than 36 weeks • Inability to initiate cooling by 6 h of age • Clinical coagulopathy • Life-threatening abnormalities of the cardiovascular or respiratory systems such as complex congenital heart disease and PPHN • Major congenital malformations, imperforate anus, suspected neuromuscular disorders, or presence of known lethal chromosomal anomaly • Death appears inevitable Mosalli R. Whole body cooling for infants with hypoxic-ischemic encephalopathy. J ClinNeonatol 2012;1:101-6.
Specific Supportive Treatment during Hypothermia • Respiratory support – assisted ventilation, keep 02 at 92-98% • Cardiovascular support • asymptomatic sinus bradycardia without cardiac dysfunction • At 33.5°C, the average HR is 80–100 beats per minutebpm • If inotropic support is required, the following regime is suggested: • Dopamine up to 10 mg/kg/min • If still hypotensive add dobutamine up to10 mg/kg/min
Specific Supportive Treatment during Hypothermia • Fluids • Start with 50–60 ml/kg/day • insert urinary catheter to measure urine output • Electrolytes • Na and Cl levels could fall duet o increased renal loss in hypothermia • Coagulation • mild derangement of blood viscosity and coagulation
Rewarming Procedure • increase the rectal temperature to 36.5–37°C at a rate not to exceed 0.5°C per hour. • final temperature goal is 36.5°C and should take about 7 hrs to achieve.
Prognosis • Infants with initial cord or initial blood pH <6.7 • 90% risk for death or severe neurodevelopmental impairment at 18 mo of age. • Apgarscores of 0-3 at 5 min, high base deficit (>20-25 mmol/L), decerebrate posture, and lack of spontaneous activity are also at increased risk for death or impairment.