Neonatology HypoxicIschemic Encephalopathy HIE Main Contents l l

  • Slides: 34
Download presentation
Neonatology: Hypoxic-Ischemic Encephalopathy, HIE

Neonatology: Hypoxic-Ischemic Encephalopathy, HIE

Main Contents l l l Clinical definition Etiology/High risk factors Pathogenesis and Pathophysiology Clinical

Main Contents l l l Clinical definition Etiology/High risk factors Pathogenesis and Pathophysiology Clinical manifestations and diagnostic Neuroimaging Prognosis Clinical Management

Clinical definition Brain damage in Fetus and neonates caused by hypoxic and/or decreasing or

Clinical definition Brain damage in Fetus and neonates caused by hypoxic and/or decreasing or abruption of blood flow to brain during perinatal period.

Etiology Almost all the factors causing asphyxia resulting HIE, and – Maternal – Placenta

Etiology Almost all the factors causing asphyxia resulting HIE, and – Maternal – Placenta and umbilicus abnormality – Substantial pulmonary, cardiac and CNS disease of the fetus and neonates – Pronged partum – Medication during delivering

High risk factors • • • Prolonged fetal bradycardia Repeated late decelerations Low Apgar

High risk factors • • • Prolonged fetal bradycardia Repeated late decelerations Low Apgar scores at 5 minutes or later Low fetal scalp or cord p. H Requirement for prolonged resuscitation with positive-pressure ventilation

Pathogenesis and Pathophysiology • Change of cerebral blood flow – normal term stable CBF:

Pathogenesis and Pathophysiology • Change of cerebral blood flow – normal term stable CBF: 50 -60 ml/min/100 g – CBF< 20 ml/min /100 g, brain damage

Pathogenesis and Pathophysiology • Change of cerebral metabolism – Increase in anaerobic glycolysis –

Pathogenesis and Pathophysiology • Change of cerebral metabolism – Increase in anaerobic glycolysis – Na +, Ca 2 + pump function intracellular ATP exhausted Na +, Ca 2 + endosmosis – Irritability amino acid blocking oxidative phosphorylation in mitochondrion – blood stream reperfusion oxygen free radical

Pathogenesis and Pathophysiology • Change of nuropathology – Term baby: cortex infarction gray matter

Pathogenesis and Pathophysiology • Change of nuropathology – Term baby: cortex infarction gray matter in partes profunda necrosis – Preterm: intraventricular haemorrhage white matter injury – Cerebral inflammation IL-1, TNF- , CKs Cellular apoptosis

Clinical manifestations • Mild – excitation/ irritability – Apparent at 24 hr – No

Clinical manifestations • Mild – excitation/ irritability – Apparent at 24 hr – No convulsion – normal EEG

Clinical manifestations • Moderate – Convulsion, 50% – with disorder of consciousness – Apparent

Clinical manifestations • Moderate – Convulsion, 50% – with disorder of consciousness – Apparent at 24 -48 hr – Deterioration: intensity of anterior fontanelle – coma

Clinical manifestations • Severe – light coma or coma at birth – Irregular respiration

Clinical manifestations • Severe – light coma or coma at birth – Irregular respiration and apnea – Convulsion with 12 hr – Poor muscle tone – Intensity of anterior fontanelle – Most die in 1 week – Survivors with severe nerosequelees

Neuroimaging Cerebral edema US

Neuroimaging Cerebral edema US

Neuroimaging Cerebral edema CT MRI

Neuroimaging Cerebral edema CT MRI

Neuroimaging US • injury in Hypothalamus and Basal ganglia

Neuroimaging US • injury in Hypothalamus and Basal ganglia

Neuroimaging injury in Hypothalamus and Basal ganglia CT MRI

Neuroimaging injury in Hypothalamus and Basal ganglia CT MRI

Neuroimaging injury in Area adjacent to the sagittal CT MR I

Neuroimaging injury in Area adjacent to the sagittal CT MR I

Neuroimaging US 早期回声增强 Cerebral artery Infarction in terms

Neuroimaging US 早期回声增强 Cerebral artery Infarction in terms

Neuroimaging Cerebral artery Infarction in terms MR I CT

Neuroimaging Cerebral artery Infarction in terms MR I CT

Neuroimaging PVL in premature US

Neuroimaging PVL in premature US

Neuroimaging PVL in premature CT MRI

Neuroimaging PVL in premature CT MRI

Neuroimaging Punctate encephalon haemorrhage MRI

Neuroimaging Punctate encephalon haemorrhage MRI

Severity and diagnosis 中华医学会儿科学会新生儿学组 2004年 11月修订; 长沙 • Mild  – Irritability, normal tone. .

Severity and diagnosis 中华医学会儿科学会新生儿学组 2004年 11月修订; 长沙 • Mild  – Irritability, normal tone. . –Moro’s: ; Sucking: normal –normal respiration,no convulsion • Moderate   –Oppressed,muscle tone ,Moro’s and Sucking –convulsion。>7 -10 d, may have sequelae • severe  –coma,frequently convulsion –irregular respiration or apnea. respiration failure. very high death rate –Survivors usually have sequelae

Prognosis • Mild and Moderate Recovered <5 d, good outcome • Middle >7 d,

Prognosis • Mild and Moderate Recovered <5 d, good outcome • Middle >7 d, or Severe worse outcome

Clinical Management • For an asphyxiated newborn: – immediate maintenance of ventilation and perfusion

Clinical Management • For an asphyxiated newborn: – immediate maintenance of ventilation and perfusion – control of seizures – maintenance of metabolic homeostasis, especially blood glucose levels to avoid additional cerebral insult

Clinical Management • Maintenance of adequate ventilation: – Avoidance of hypoxemia and hypercapnia •

Clinical Management • Maintenance of adequate ventilation: – Avoidance of hypoxemia and hypercapnia • To avoid systemic hypotension – cerebral perfusion • Prevention of fluid overload: – current data in human newborns do not provide convincing evidence that supports the use of antiedema therapy • Maintenance of normoglycemia

Clinical Management • Control seizures – begin with a loading dose of phenobarbital (20

Clinical Management • Control seizures – begin with a loading dose of phenobarbital (20 mg/kg) , IV – followed by additional 5 -mg/kg, total dose 40 mg/kg • For refractory seizures: – lorazepam by IV may be indicated • Recent recommendations emphasis: – brief duration of treatment; possible deleterious effects of anticonvulsants on the developing nervous system.

Clinical Management • Cool Cap (Selective Head Hypothermia Therapy) – Multi-center trial: – US,

Clinical Management • Cool Cap (Selective Head Hypothermia Therapy) – Multi-center trial: – US, Canada, UK and New Zealand: 25 – Sample: trial/control=116/118 • Apgar<=6/5 min+Cord arterial ph <7. 1 • clinical HIE+EEG abnormal – a. EEG severe: (n=46):not effective – a. EEG Moderate : (n=172); showed protective Gluckman PD, Cool Cap trial group. Lancet 2005

Clinical Management • Cool Cap (Selective Head Hypothermia Therapy) • a. EEG Moderate :

Clinical Management • Cool Cap (Selective Head Hypothermia Therapy) • a. EEG Moderate : (n=172); showed protective – Death rate: – severe neromotion disabled 48% vs 66% p=0. 02 – Bayley MDI: 85 vs 77 p=0. 04 – Bayley PDI: 90 vs 85 p=0. 047 Gluckman PD, Cool Cap trial group. Lancet 2005

Clinical Management • • Whole body Hypothermia NIH Neonatal Network, US Multi-center: 16, sample:

Clinical Management • • Whole body Hypothermia NIH Neonatal Network, US Multi-center: 16, sample: 208 Results; – Death: 24%(H) vs 36% p=0. 08 – middle or severe disabled • 45%(H) vs 62%(N) p=0. 01 (OR: 0. 72, 95% CI 0. 55 -0. 93) Shankaran et al:National Institute of Child Health and Human Development Neonatal Research Network. Whole -body hypothermia for neonates with hypoxic-ischemicencephalopathy. NEJM 2005 Oct 13; 353(15): 1574 -84.

Summery • HIE is the major cause of the neonatal death • Asphyxia and

Summery • HIE is the major cause of the neonatal death • Asphyxia and ischemia hypoxemia in perinatal resulting in HIE • Diagnosis based on clinical manifestation and may combined with Neuroimaging • Though there are some therapies for HIE treatments for HIE is still not as effective as expected

Thanks and questions?

Thanks and questions?