Neonatology HypoxicIschemic Encephalopathy HIE Main Contents l l
- Slides: 34
Neonatology: Hypoxic-Ischemic Encephalopathy, HIE
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 abruption of blood flow to brain during perinatal period.
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 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: 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 – 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 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 convulsion – normal EEG
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 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 CT MRI
Neuroimaging US • injury in Hypothalamus and Basal ganglia
Neuroimaging injury in Hypothalamus and Basal ganglia CT MRI
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 Cerebral artery Infarction in terms MR I CT
Neuroimaging PVL in premature US
Neuroimaging PVL in premature CT 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. . –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, or Severe worse outcome
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 • 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 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, 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 : (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: 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 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?
- Lectures paediatrics
- History of neonatology
- Main contents
- Apgar
- Terminology services
- Simone hie
- Iap slides
- Perinatal asphyxia
- Kansas hie
- Open hie
- Roshini jayasankar
- Hie transistor
- Irhmis
- Akaims
- Open hie
- Camden hie
- Viewpage
- Albert camus tujec
- Hashimoto encephalopathy diagnostic criteria
- Hepatic encephalopathy staging
- Uremic encephalopathy
- Encephalopathy stages
- Increase bp
- West haven hepatic encephalopathy
- Hepatic encephalopathy pathophysiology
- Encephalopathy stages
- Cholycystostomy
- J'overt
- Mdcalc childs pugh
- Asterixis in hepatic encephalopathy
- Hepatic encephalopathy management
- Bilirubin encephalopathy
- Hepatic encephalopathy staging
- Acute toxic encephalopathy icd 10
- Normal bun