Transcript Document 7173466
Neonatology: Hypoxic-Ischemic Encephalopathy, HIE
Main Contents
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 pH Requirement for prolonged resuscitation with positive-pressure ventilation
Pathogenesis and Pathophysiology
•
Change of cerebral blood flow
–
normal term stable CBF: 50-60ml/min/100g
–
CBF
＜
20ml/min /100g, brain damage
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 mitochondrion blood stream reperfusion
radical
oxygen free
Pathogenesis and Pathophysiology
•
Change of nuropathology
–
Term baby: cortex infarction gray matter in partes profunda necrosis
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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%
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with disorder of consciousness
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Apparent at 24-48 hr
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Deterioration: intensity of anterior fontanelle
–
coma
Clinical manifestations
•
Severe
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light coma or coma at birth
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Irregular respiration and apnea
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Convulsion with 12 hr
–
Poor muscle tone
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Intensity of anterior fontanelle
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Most die in 1 week
–
Survivors with severe nerosequelees
HIE
的诊断
—
临床表现
中华医学会儿科学会新生儿学组
2004
年
11
月修订
;
长沙 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。
HIE
的诊断
—
脑电图
• • • • 中华医学会儿科学会新生儿学组 2004年11月 长沙修订 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 背景活动异常
(
落后于实际胎龄
)
，
(
以低电压和爆发抑制为主
)
振幅整合脑电图
(aEEG)
HIE
的诊断
—
影象学检查
• • • 中华医学会儿科学会新生儿学组
2004
年
11
月修订
;
长沙 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
Cerebral edema
Neuroimaging
US
Cerebral edema
Neuroimaging
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
CT MR I
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
。
>7-10d, 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 <5d, good outcome
•
Middle >7d,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:
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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 (20mg/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<=6/5min+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
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
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