Hypoxic- ischemic encephalopathy HIE

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Hypoxic- ischemic
encephalopathy
HIE
Lin Niyang
Pediatric Department of the First affiliated hospital of Shantou University Medical College
Basic Concepts
*is a kind of brain injuries in fetus and
neonates due to hypoxia and decline
of cerebral blood flow during perinatal
period.
*has characteristic pathophysiological
process and nerve pathological
changes.
*has a series of clinical encephalopathy performances.
*can leave nervous system sequelae.
1. Etiology
2. Pathogenesis
※3. Clinical manifestations and degrees
4. Diagnosis
5. Differential diagnosis
※6.Treatment
7. Prognosis
8. Prevention
Etiology
Key: Anoxia
Anoxia link:
mother
placenta
umbilical cord
fetus and neonates
Anoxia time:
before birth
during birth
before and during birth
after birth
20%
35%
35%
10%
Pathogenesis
1 Changes of brain blood dynamics
2 Changes of brain energy metabolism
3 Nervous pathological changes
1 The changes of brain blood dynamics
1.1 Incomplete anoxia:
1stThe whole body blood recontribution
→ The blood flow to heart, brain, adrenal glands↑
to the kidney, lung, skin, stomach and intestines↓
2nd Persistent anoxia→ system blood pressure ↓
→ The blood flow to brain ↓
→The brain blood recontribution ( to guarantee the
function of the important part:The thalamus, brain stem,
hippocampi, cerebellum).
3rd Persistent lacking of the blood flow
→ nervous cell injury.
1 The changes of brain blood dynamics
1.2 Acute complete anoxia:
Thalamus, brain stem and cerebellum are
the vulnerable areas, however, the cerebral
hemisphere are normal.
1.3 Dysfunction of the
cerebraovascular regulation:
Caused by hypoxia and acidosis;
lead to cerebral blood flow unstable:
BP↑→hemorrage around ventricular
BP↓→brain blood flow↓
2 The changes of brain energy metabolism
Ca++ overload
Excitatory amino acids
Free radicals
Neural necrosis and apoptosis
3 The nerve pathological changes
Early period: 7 ~ 10 days
edema, hemorrhage
Later period: after 10 days
necrosis, liquefaction,bubble, atrophy
Sequelae period:
neuron number reduces
neuron dysfunction
formation of the myelin sheath reduces
periventricular leukomalacia(PVL)
Clinical manifestations
and degrees
Mild degree
Moderate degree
Severe degree
1.Consciousness
2.Muscle tension
3.Primary reflex:
Moro reflex
Sucking reflex
4.Convulsion
5.Central respiratory failure
6.Pupil change
7.Anterior fontanel tension
8.Duration and prognosis
Assistant examinations
Blood analysis:
Blood electrolyte, ion,blood gas,et al.
To detect the function of the heart, lung,
kidney, liver, GI.
Image diagnosis:
The skull B ultrasound, CT, MRI.
Others:
ECG, EEG.
B ultra
HIE急性期
HIE恢复期
HIE后遗症期
CT
HIE急性期
HIE后脑室周围白质软化
HIE后外部性脑积水
HIE后脑萎缩
Diagnosis
1 History:
Anoxia causes, occurrence time, degree
2 Symptoms:
Consciousness, expression of the eyes,
reaction, convulsion, et al.
3 Signs:
R, HR, BP, skin color, pupil reaction,
anterior fontanel tension, muscle tension,
Moro reflex,sucking reflex
NBNA(Neonatal Behavioral Neurological
Assessment):
normal >37,abnormal <35
4. Assistance examination:
Blood analysis:CK-BB
Image:The skull B ultrasound, CT, MRI.
Others: ECG, EEG.
Differential Diagnosis
1. Congenital viral infection
2. Genetic and metabolic disease
3. Parasitic infection
Treatment
1. Treatment during the earlier period
2. Treatment during the later period
1.Treatment during the earlier period
(0~10 days)
0~3d:
Aim—
To maintain the internal environment stability
Three ways to support life
①To maintain normal ventilation so as
to maintain normal PaO2, PaCO2 and pH;
②To maintain normal circulation,
which means to maintain normal heart
rate (HR) and blood pressure(BP);
③To maintain normal blood glucose
(4.16~5.55mmol/L)
Three ways to control the Symptoms:
①To control convulsion:Luminal,
Valium, chloralhydrate
②To decrease the intracranial
pressure:Lasix, 20%Mannitol
③To eliminate the symptoms of the
stem damage:naloxone
1.Treatment during the earlier period
(0~10 days)
4~10d:
Aim—
To improve the cerebral blood flow
To promote cerebral metabolism
To recovery the neural system function
2. Treatment during the later period
Sequelae manifestations:
cerebral palsy
epilepsy
mental retardation
To promote cerebral function recovery
To make early intervention
To follow-up regularly
Prognosis
Prognosis
Apgar score;
 Consciousness;
 Intrauterine distress;
 Persistent coma;
 Abnormal EEG;
 Abnormal BAEP;
 Severe cranial CT and B-ultra changes;
 CK-BB increasing;
 NBNA

Prevention
Prevention
 Before
birth:
 During birth:
 After birth:
Reference:
新生儿缺氧缺血性脑病诊断依据和临
床分度
中华儿科杂志,1997,15(2):99100
Main points
1 What is HIE?
2 The causes of HIE.
*3 The clinical manifestations and the
degrees of HIE.
*4 The treatment principles of HIE?
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