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Intracranial hemorrhage and brain disorders

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Presentation on theme: "Intracranial hemorrhage and brain disorders"— Presentation transcript:

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2 Intracranial hemorrhage and brain disorders
William 2001

3 Intraventricular hemorrhage
Brain disorders Cerebral palsy Neonatal encephalopathy

4 intraventricular Hemorrhage
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 - Postnatal factors: RD Ventilation therapy PCO2 ≥ 60 mmHg
Heparin  X 4 Hg - Postnatal factors: RD Ventilation therapy PCO2 ≥ 60 mmHg within 1st 2 hours PO < 40 mmHg 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 - MgSO4 ↓ 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 Brain disorders 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 Cerebral palsy 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 % Diplegia % Hemiplegia % 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: = 0. 1 - 0
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 < 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 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 ↓O2

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: of infants who need resuscitation
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 1st 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 MgSO4: 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: - 1st 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 Neonatal encephalopathy
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 1st 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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