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Hypoxic- ischemic encephalopathy HIE

Hypoxic- ischemic encephalopathy HIE. Lin Niyang Pediatric Department of the First affiliated hospital of Shantou University Medical College.

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Hypoxic- ischemic encephalopathy HIE

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  1. Hypoxic- ischemic encephalopathyHIE Lin Niyang Pediatric Department of the First affiliated hospital of Shantou University Medical College

  2. Basic Concepts*is a kind of brain injuries in fetus and neonates due to hypoxia and decline of cerebral blood flowduring perinatal period.*has characteristic pathophysiological process and nerve pathological changes. *has a series of clinical encephalo-pathy performances. *can leave nervous system sequelae.

  3. 1. Etiology 2. Pathogenesis※3. Clinical manifestations and degrees 4. Diagnosis 5. Differential diagnosis※6.Treatment 7. Prognosis 8. Prevention

  4. Etiology

  5. Key: Anoxia Anoxia link:mother placentaumbilical cordfetus and neonatesAnoxia time: before birth 20% during birth 35% before and during birth 35% after birth 10%

  6. Pathogenesis

  7. 1 Changes of brain blood dynamics 2 Changes of brain energy metabolism 3 Nervous pathological changes

  8. 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.

  9. 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↓

  10. 2 The changes of brain energy metabolism Ca++ overload Excitatory amino acids Free radicals Neural necrosis and apoptosis

  11. 3 The nerve pathological changes Early period: 7 ～ 10 days edema, hemorrhageLater period: after 10 days necrosis, liquefaction,bubble, atrophySequelae period: neuron number reduces neuron dysfunction formation of the myelin sheath reducesperiventricular leukomalacia(PVL)

  12. Clinical manifestations and degrees

  13. Mild degreeModerate degreeSevere degree

  14. 1.Consciousness2.Muscle tension3.Primary reflex: Moro reflex Sucking reflex4.Convulsion5.Central respiratory failure6.Pupil change7.Anterior fontanel tension8.Duration and prognosis

  15. Assistant examinations

  16. 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.

  17. B ultra HIE急性期 HIE后遗症期 HIE恢复期

  18. CT HIE急性期 HIE后外部性脑积水 HIE后脑室周围白质软化 HIE后脑萎缩

  19. Diagnosis

  20. 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

  21. 4. Assistance examination: Blood analysis:CK-BB Image:The skull B ultrasound, CT, MRI. Others: ECG, EEG.

  22. Differential Diagnosis

  23. 1. Congenital viral infection2. Genetic and metabolic disease3. Parasitic infection

  24. Treatment

  25. 1. Treatment during the earlier period2. Treatment during the later period

  26. Treatment during the earlier period (0~10 days)0～3d：Aim—To maintain the internal environment stability

  27. Three ways to support life①To 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)

  28. 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

  29. 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

  30. 2. Treatment during the later periodSequelae manifestations: cerebral palsy epilepsy mental retardation To promote cerebral function recoveryTo make early interventionTo follow-up regularly

  31. Prognosis

  32. Prognosis • Apgar score; • Consciousness; • Intrauterine distress; • Persistent coma; • Abnormal EEG; • Abnormal BAEP; • Severe cranial CT and B-ultra changes; • CK-BB increasing; • NBNA

  33. Prevention

  34. Prevention • Before birth: • During birth: • After birth:

  35. 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）：99-100Reference: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）：99-100

  36. Main points1 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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