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William 2001  Intraventricular hemorrhage  Brain disorders  Cerebral palsy  Neonatal encephalopathy.

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Presentation on theme: "William 2001  Intraventricular hemorrhage  Brain disorders  Cerebral palsy  Neonatal encephalopathy."— Presentation transcript:

1

2 William 2001

3  Intraventricular hemorrhage  Brain disorders  Cerebral palsy  Neonatal encephalopathy

4 Types of intracranial Hg:  Subdural  Subarachnoid  Intracerebellar  Periventricural - intraventricural : -- In term infants: ½ due to trauma/asphyxia ¼ due to unknown causes

5 -- In preterm infants: Due to multifactorial factors:  Hypoxic - ischemic  Anatomical causes  Coagulopathy Periventricular – intraventricular Hg: - Fragile capillaries in germinal matrix rupture  Hg

6 - May extend to the ventricles or brain parenchyma - Common in neonates < 34 weeks but may occur in older infants - Starts usually within 72 hours but may develop 24 days after birth - External perinatal and postnatal factors may alter it’s % and severity

7 - Minimal in ½ of the cases  no C/P - Mostly small Hg or Hg confined to the ventricles  resolve without neurological impairment - In large Hg  hydrocephalus or periventricular leukomalacia  CP Pathology: - Due to damage of germinal matrix

8 capillary network - ↑ in preterm infants due to:  Poor support  Venous anatomy in this area  stasis  Hg  Vascular autoregulation is impaired < 32 weeks

9 Extensive Hg  death or handicap due to periventricular leukomalacia: = Cystic area due to ischemia or Hg Incidence and severity: = 4% in term infants = ½ infants < 32 weeks are born with some Hg  minimal effect

10 Very LBW have the:  Earliest onset  Greatest progression  Highest mortality rate Assessed by: U/S and CT

11 Grades: I matrix Hg II intraventricular Hg III dilatation of the ventricles IV parenchymal Hg Survival: > 90% in I & II % handicap 50% in III & IV

12 Very LBW infants: 45% intraventricular Hg 20% of them are III & IV degree Contributing factors: - Prematurity and it’s complications:  Infection  ischemia  Acidosis  X 3 ↑ risk for grade III & IV if pH < 7.2  RD and mechanical ventilation

13  Heparin  X 4 Hg - Postnatal factors:  RD  Ventilation therapy  PCO 2 ≥ 60 mmHg within 1 st 2 hours  PO 2 < 40 mmHg within 1 st 2 hours  Pneumothorax

14 Treatment: 1 - Antenatal corticosteroids:  ↓ mortality ↓ RD ↓ intraventricular Hg + benefit in cases of PROM Betamethasone  ↓ leukomalacia compared to dexamethasone

15 2 – Phenobarbital and vit K = controversial 3 - Vit E  ↓ severity and % but does not ↓ mortality 4 - Indomethacin  ↑ mortality in infants < 1000 gm 5 - MgSO 4  ↓ periventricular Hg

16 Prevention:  Avoid hypoxia  CS in preterm cephalic fetus  no evidence Studies: - No significant difference - ↓ early intracranial Hg

17 Outcome in extreme prematurity:  ↑ mortality  ↑ neurological injury  ↑ ophthalmological injury  ↑ pulmonary injury Age α 1 / severe neurological abnormalities

18 1862 = abnormal labor  spasticity 1900 = Sigmund Freud  many abnormalities can  spastic rigidity Cerebral palsy is caused by a combination of:  Genetic factors  Environmental factors  Physiological factors  Obstetric factors

19 Still many doctors are afraid of CP from obstetric factors  ↑ CS to 1 : 4 births in US with no ↓ in CP

20 Asphyxia:  Profound metabolic or mixed acidemia < 7  Persistent Apgar score 0 – 3 for > 5 min  Neurological sequelae: - Seizures - Coma - Hypotonia - Dysfunction of ≥ 1 system : GIT - Cardiac – Hematologic – respiratory

21 Causes of low Apgar score alone:  PTL  Maternal sedation  Anesthesia  Vigorous suction or intubation  Congenital anomalies  Newborn diseases as: neurological musculoskeletal - cardiorespiratory

22 Definition: Nonprogressive motor disorder of early infant onset in ≥ 1 limbs  spasticity or paralysis ± MR / epilepsy ( not associated with perinatal asphyxia in the absence of CP ) Categorized by:  Type of neurological dysfunction : Spastic – dyskinetic - ataxic

23  Number and distribution of involved limbs : Quadriplegia 20% Diplegia 35% Hemiplegia 30% Monoplegia Major types of CP: Spastic quadriplegia (↑in MR and seizures) Diplegia  ↑ in LBW and preterm Hemiplegia - Choreoathetoid - Mixed

24 25% of CP + MR ( IQ < 50% ) Incidence and epidemiology: = % of live birth (↑ by ↑ survival of LBW) = 0.27 % at age 5 – 7 years = 1.5 % < 2500 gm = 1.3 – 9 % from 500 – 1500 gm = 50 % < 25 weeks

25 Risk factors:  Genetic - Maternal MR - Microcephaly - Congenital anomalies  < 32 weeks  < 2000 gm  infection

26 Obstetric complications:  Not strongly predictive of CP  20% + perinatal asphyxia  50% + LBW – congenital anomalies – microcephaly and others  No single intervention can prevent CP  Most cases of CPs  unknown cause Study: 25% of CP is due to NTD or postnatal causes as infection or injury

27 Strongest predictors for CP:  Congenital anomalies  LBW  Low placental weight  Abnormal fetal position as: breech or transverse lie - No correlation between CS or instrumental delivery with CP - < 1000 gm  only early GA

28 and LBW correlate with neonatal neurological morbidity Intrapartum events:  No special FHR pattern in CP  Continuous electronic monitoring equals intermittent monitoring  75% of CP are unavoidable  Abnormal FHR = preexisting neurological abnormalities

29  92% of CP + no intrapartum injury 3% + “”””” is possible 5% + “”””” is likely  Since 1965 CS ↑  1 : 4 in US but % of CP is still the same Study: Electronic monitoring  ↑ CP in preterm infants # intermittent auscultation

30 Apgar score: -  poor predictors of CP except in: - Complicated birth + 5m Apgar score = ≤ 3  ↑ death + ↑ CP - Uncomplicated birth + 5m Apgar score = ≤ 3  no ↑ risk - Most neurological abnormalities are due to factors other than perinatal ↓O 2

31 - LBW + 1 m Apgar score ≤ 3  ↑ death X 5 + ↑ CP X 3 - Low 5 m Apgar score is predictive of neurological impairment - < 37 weeks completed + 5 m Apgar score ≤ 3  X 75 fold death - ≥ 38 weeks + 5 m Apgar score ≤ 3  X 1460 fold death within 28 days

32 - Low 1 & 5 m Apgar score alone are:  Excellent predictors for identification of infants who need resuscitation  Insufficient evidence that the damage is due to hypoxia Umbilical cord blood gas :  If no metabolic acidosis  intrapartum hypoxia or asphyxia is excluded

33  Alone U/C pH is not superior to Apgar score in predicting long – term neurological D  Most neurological diseases are associated with normal pH + low Apgar score = hypoxia is not a major cause of long – term neurological morbidity  Neither pH nor acidemia correlate with long term neurological disease in term infants

34  The cutoff for clinically significant acidemia is now pH < 7.0 instead of < 7.2  If pH is ≤ 7  only 7% of infants develop mild neurological sequelae The use of pH to assess predictability of neonatal death within 28 days:  ≤ 7 + Apgar score ≤ 3  3204 relative risk  < 6.8  ↑ death X 1400 fold

35 Nucleated RBCs:  ↑ in hypoxia  Number of NRBCs α degree of hypoxia and can determine it’s duration Studies :  ↑ NRBCs is associated with asphyxia  No relation between hypoxia and NRBCs  NRBCs are hematological markers of maternal and neonatal infection as well placental histological evidence of infection

36  Neonatal serial lymphocyte and normoblast count may accurately identify the time before birth when encephalopathy occur: peak 2 hours after injury and normalize in 24 – 36 hours Periventricular leukomalacia:  Cyctic areas after hemorrhgic infarction  Ischemia  necrosis  cyst in 2 weeks to 104 days

37  Severe ICHg and periventricular leukomalacia may  CP  40% of LBW develop CP and III or IV degree ICHg  Risk of CP ↑ X 16 in III and IV degree ICHg  ≤ 34 weeks 11% of transient cysts  CP 67% of localized cysts  CP 100% of extensive cysts  CP  Size of the cyst α ↑ CP risk

38  Symmetrical cysts = highest risk  Periventricular leukomalecia is linked more than ICHg to infection as: - Chorioamnionitis - Prolonged PROM - Neonatal hypotension  Periventricular leukomalacia is associated with:

39  1 st trimester Hg  UTI at labor  LBW  Smoking  PTL  Neonatal acidosis  Meconium staining  >72 hours of ritodrine therapy

40 Preterm periventricular leukomalacia: Blood supply to the brain < 32 weeks: 1 - Ventriculopedal system:  penetrates into the cortex 2 - Ventriculofugal system:  reaches down to the ventricles then curves upward

41 In between the 2 systems the area near the lateral ventricles where the pyramidal tract pass = watershed area because there is no anastomosis between the 2 systems > 32 weeks blood supply shifts away from the brain stem and basal ganglia toward the cortex Effect of ischemia: < 32 weeks  spastic diplegia > 32 weeks  brain damage

42 Perinatal infection: Maternal or intrauterine infection  endotoxin  ↑ cytokines  ↑ PGn  PTL  ICHg & PVL  CP

43 ↑ Cytokines 1, 6, 8, TNF   Direct toxic effect on oligodendrocytes and myelin  Vessel rupture  tissue hypoxia and massive cell death  ↑ glutamate  - white matter damage - ↑ intracellular Ca  toxic - Direct toxic effect on oligodendroglia

44 Studies:  E Coli injection into animal embryo  brain damage  TNF and IL 6 ↑ in brains of infants with PVL  AF culture: 45% of CP  microorganisms 85% of CP  ↑ IL 6 - 8

45  PTL after PROM # PTL caused by other causes: ICHg and PVL ↑ after spontaneous labor ↑ after spontaneous ROM Both if + chorioamnionitis  ↑ CP  Most significant clinical correlates of white matter necrosis in preterm infants : - Funistis - Purulent AF - Placental vessel abnormalities

46  > 2500 gm fetus + maternal fever or chorioamnionitis  X 9 CP + neonatal infection  X 19 CP Prevention :  Corticosteroid therapy  Aggressive treatment or prophylaxis of infection in women delivering preterm infants = neuroprotective

47  MgSO 4:  Stabilizes vascular tone  ↓ fluctuations of cerebral blood flow  ↓ reperfusion injury  ↓ cytokines and bacterial endotoxins  ↓ inflammatory effects of infection  blocks Ca intracellular toxic effect Limited to preeclampsia

48 Neuroradiological imaging: CT: 25% of CP  normal CT 70% of preterm infants  early insult 50% of term infants  prenatal insult:  37% periventricular leukomalacia  17% maldevelopment  19% cortical or subcortical injury

49 MRI: - 80% of preterm CP  periventricural white matter damage = hypoxic ischemic - 50% of term CP  antenatal damage as:  Gyral abnormalities as polymicrogyria = midpregnancy injury  Isolated periventricular leukomalacia In 25% of these cases, MRI + C/P are suggestive of hypoxic ischemic insult

50 MRI can predict the specific pattern of neurophysiological dysfunction by:  Severity of dilatation  Degree and extent of white matter loss  Involvement of optic structures  Thinning of corpus collosum MRI can determine the most likely time of brain insult in CP

51 U/S: - 1 st day U/S diagnose antenatal insult intraventricular Hg = secondary injury that developed in the nursery - Results of U/S differ than MRI but complementary to it

52 Definition: Disturbed neurological function in the earliest days of life in term infants Clinical picture:  Respiratory depression  Hypotonia  Subconsciousness  Seizures Due to hypoxic ischemic insult of unknown time

53 Mild E:  Hyperalertness  Irritability  Jitteriness  Hypo/hypertonia Moderate E:  Lethargy  Severe hypotonia  Occasional seizures

54 Severe E:  Coma  Recurrent apnea  Multiple seizures Normal neurological outcome :  Mild E  all  Moderate E  80%  Severe E  all

55 Studies: - High risk term and preterm neonates:  30% neonatal E  17% cognitive and motor deficits:  ¼ mild – moderate E  ½ severe E - Respiratory complications are the most common risk factor

56 - Perinatal hypoxia is associated with:  26% of mild – moderate E  66% of severe E - Serial head circumflex in E: If ↓ > 3.1% relative to that expected for age in the 1 st 4 months = predicts microcephaly with 90% specificity

57 Mental retardation: % Isolated MR (=MR without CP or epilepsy) is associated with perinatal hypoxia in < 5% Seizure disorders: - Isolated seizure disorders or epilepsy are not usually caused by perinatal hypoxia

58 - Major predictors are:  Congenital anomalies  Family history  Neonatal seizures


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