Therapeutic hypothermia for neonatal hypoxic-ischemic encephalopathy
Neonatology: Hypoxic-Ischemic Encephalopathy, HIE.
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Transcript of Neonatology: Hypoxic-Ischemic Encephalopathy, HIE.
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Neonatology: Hypoxic-Ischemic Encephalopathy, HIE
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Main Contents
Clinical definition Etiology/High risk factors Pathogenesis and Pathophysiology Clinical manifestations and diagnostic N
euroimaging Prognosis Clinical Management
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Clinical definition
Brain damage in Fetus and neonates caused by hypoxic and/or decreasing or abruption of blood flow to brain during perinatal period.
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Etiology
Almost all the factors causing asphyxiaresulting HIE, and – Maternal– Placenta and umbilicus abnormality – Substantial pulmonary, cardiac and
CNS disease of the fetus and neonates– Pronged partum – Medication during delivering
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High risk factors
• Prolonged fetal bradycardia
• Repeated late decelerations
• Low Apgar scores at 5 minutes or later
• Low fetal scalp or cord pH
• Requirement for prolonged resuscitation with positive-pressure ventilation
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Pathogenesis and Pathophysiology
• Change of cerebral blood flow– normal term stable CBF: 50-60ml/min/100g– CBF < 20ml/min /100g, brain damage
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Pathogenesis and Pathophysiology
• Change of cerebral metabolism– Increase in anaerobic glycolysis– Na +, Ca2 + pump function intracellular ATP exhausted Na +, Ca2 + endosmosis– Irritability amino acid blocking oxidative phosphorylation in mito
chondrion – blood stream reperfusion oxygen free
radical
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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
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Clinical manifestations
• Mild – excitation/ irritability– Apparent at 24 hr – No convulsion – normal EEG
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Clinical manifestations
• Moderate – Convulsion, 50%– with disorder of consciousness – Apparent at 24-48 hr – Deterioration: intensity of anterior fontanell
e – coma
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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
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HIE的诊断—临床表现
1. 胎儿宫内窒息史,严重的胎儿宫内窘迫表现 ( 胎心< 100 次,持续 5 分钟以上;和 / 或羊水 III 度污染 )
2. 出生时有重度窒息 :( Apgar 评分 1分钟≤ 3分) 至 5 分钟时仍≤ 5 分;或出生时脐动脉血气 pH ≤ 7.00 ;3、出生后 24 小时内出现神经系统表现;4、排除低钙血症、低糖血症、感染、产伤和颅内出血等引 起的抽搐,以及遗传代谢性疾病和其他先天性疾病所引 起的神经系统疾患。
•同时具备以上 4条者可确诊,第 4条暂时不能确定者作为 拟诊病例。
中华医学会儿科学会新生儿学组 2004年 11月修订 ; 长沙
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HIE的诊断—脑电图
• 在生后 1周内检查• 脑电图异常程度与临床分度基本一致• 脑电图异常表现: 脑电活动延迟 (落后于实际胎龄 ), 背景活动异常 (以低电压和爆发抑制为主 )• 振幅整合脑电图 (aEEG)
中华医学会儿科学会新生儿学组 2004 年 11 月 长沙修订
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HIE的诊断—影象学检查
• 头颅 B超 可在 HIE病程早期 (72小时内 ) 开始检查 有利于了解脑水肿、基底神经节丘脑损伤 和脑动脉梗死等病理改变• CT 生后 4-7天为宜• MRI 对 HIE病变性质与程度评价方面优于 CT
中华医学会儿科学会新生儿学组 2004年 11月修订 ; 长沙
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US
Cerebraledema
Cerebraledema
Neuroimaging
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CT MRI
Cerebral edema
Cerebral edema
Neuroimaging
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• injury in Hypothalamus and Basal ganglia
US
Neuroimaging
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CT
MRIMRI
injury in Hypothalamus and Basal ganglia
Neuroimaging
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MRMR ICTCT
injury in Area adjacent to the sagittal
Neuroimaging
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Cerebral arteryInfarction in terms
早期回声增强
US
Neuroimaging
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Cerebral arteryInfarction in terms CTCT
MRMR I
Neuroimaging
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PVL in premature
US
Neuroimaging
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PVL in premature
CTCT
MRI
Neuroimaging
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Punctate encephalon haemorrhage
MRI
Neuroimaging
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Severity and diagnosis
• Mild – Irritability, normal tone..–Moro’s: ; Sucking: normal–normal respiration , no convulsion
• Moderate –Oppressed,muscle tone ,Moro’s and Sucking –convulsion。 >7-10d, may have sequelae
• severe –coma, frequently convulsion–irregular respiration or apnea. respiration failure. very high death rate –Survivors usually have sequelae
中华医学会儿科学会新生儿学组 2004年 11月修订 ; 长沙
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Prognosis
• Mild and Moderate
Recovered <5d, good outcome
• Middle >7d,or Severe
worse outcome
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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
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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 c
onvincing evidence that supports the use of antiedema therapy
• Maintenance of normoglycemia
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Clinical Management
• Control seizures– begin with a loading dose of phenobarbital (20mg/
kg) ,IV– followed by additional 5-mg/kg, total dose 40 mg/k
g
• For refractory seizures: – lorazepam by IV may be indicated
• Recent recommendations emphasis: – brief duration of treatment; possible deleterious ef
fects of anticonvulsants on the developing nervous system.
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Clinical Management
• Cool Cap (Selective Head Hypothermia Therapy)
– Multi-center trial :– US, Canada, UK and New Zealand: 25– Sample: trial/control=116/118
• Apgar<=6/5min+Cord arterial ph <7.1• clinical HIE+EEG abnormal
– aEEG severe: (n=46) : not effective– aEEG Moderate : (n=172); showed protective
Gluckman PD, Cool Cap trial group. Lancet 2005
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Clinical Management
• Cool Cap (Selective Head Hypothermia Therapy)
• aEEG 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
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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.
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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
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Thanks and questions?