Hypoxic IschemicEncephalopathy         Prof. Saad S Al-Ani     Senior Pediatric Consultant    Head of Pediatric Department...
DefinitionsAnoxia is a term used to indicate the consequences of complete lack of oxygen as aresult of a number of primary...
Hypoxic-ischemic encephalopathy  Is an important cause of permanentdamage to CNS cells that may result inneonatal death or...
Fifteen to 20% of infants with hypoxic-ischemic encephalopathy die in the neonatalperiod    25-30% of survivors are left w...
Effects of Asphyxia                  System                  Effect  I. Central nervous system                            ...
Effects of Asphyxia               System Effect               (cont.)  III. Pulmonary                                     ...
Effects of Asphyxia                   System Effect                   (cont.)VII. Metabolic1. Inappropriate secretion of a...
Asphyxia       is considered in infants with:  1.     Fetal acidosis (pH <7.0)  2.    A 5-min Apgar score of 0-3  3.    Hy...
Causes Of Fetal Hypoxia    (1) Inadequate oxygenation of maternal        blood         as a result of:              I. Hyp...
Causes Of Fetal Hypoxia             (cont.)    (3) Inadequate relaxation of the uterus         to permit placental filling...
Causes Of Fetal Hypoxia             (cont.)      (5) Impedance to the circulation of blood         through the umbilical c...
Fetal hypoxia    Abnormal Doppler velocimetry .    On an umbilical artery Doppler flow velocity waveform   The umbilical p...
Causes of after birth hypoxia  (1)Anemia severe enough to lower the oxygen content of the blood to     a critical level, a...
Causes of after birth hypoxia (cont.) (3) Deficit in arterial oxygen saturation    from failure to breathe adequately post...
PathophysiologyWithin minutes of the onset of total fetal hypoxia :  1.Bradycardia  2. Hypotension  3. decreased cardiac o...
Patterns of periodic fetal heart rate (FHR)deceleration        A shows early deceleration occurring during the peak of ute...
Patterns of periodic fetal heart rate(FHR) deceleration (cont . )              B, Late deceleration caused by uteroplacent...
Patterns of periodic fetal heart rate(FHR) deceleration (cont.)       C, Variable deceleration as a result of umbilical co...
Clinical Manifestations  Hypoxic-Ischemic Encephalopathy in Term  Infants    Signs:   Stage 1        Stage 2    Stage 3   ...
Clinical Manifestations  Hypoxic-Ischemic Encephalopathy in Term  Infants (cont.)  Signs:            Stage 1              ...
Clinical Manifestations  Hypoxic-Ischemic Encephalopathy in Term  Infants (cont.)  Signs:          Stage 1                ...
Clinical Manifestations  Hypoxic-Ischemic Encephalopathy in Term  Infants (cont.)  Signs:          Stage 1                ...
Treatment Therapy is supportive and directed at the organ system manifestations   Careful attention to :   •   Ventilatory...
Treatment           (cont.)   No established effective treatment is available for the brain tissue injury,    although man...
Treatment          (cont.)    Seizure activity may be severe and refractory to the usual    doses of anticonvulsants    Ph...
Prognosis    The outcome of hypoxic-ischemic encephalopathy ranges from    complete recovery to death     The prognosis de...
Prognosis          (Cont.)     Severe encephalopathy characterized by :         1.Flaccid coma         2.Apnea         3.A...
Prognosis          (Cont.)    1. A low Apgar score at 20 min     2. Absence of spontaneous respirations at 20 min of age  ...
Prognosis            (Cont.)Brain death after neonatal hypoxic-ischemic encephalopathy is diagnosed by: 1. Clinical findin...
Thank you05/26/2010      Khorfakkan Hospital Pediatric Department                                                30
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hypoxic ischemic encephalopathy

  1. 1. Hypoxic IschemicEncephalopathy Prof. Saad S Al-Ani Senior Pediatric Consultant Head of Pediatric Department Khorfakkan Hospital . Sharjah saadsalani@yahoo.com
  2. 2. DefinitionsAnoxia is a term used to indicate the consequences of complete lack of oxygen as aresult of a number of primary causes Hypoxia refers to an arterial concentration of oxygen that is less than normal Ischemia refers to blood flow to cells or organs that is insufficient to maintain their normal function Biagioni E, Mercuri E, Rutherford M, et al: Combined use of electroencephalogram and magnetic resonance imaging in full-term neonates with acute encephalopathy. Pediatrics 2001;107:461 05/26/2010 Khorfakkan Hospital Pediatric Department 2
  3. 3. Hypoxic-ischemic encephalopathy Is an important cause of permanentdamage to CNS cells that may result inneonatal death or be manifested lateras cerebral palsy or mental deficiency Nelson Textbook of Pediatrics 19th ed.2010 . pages 566 - 56805/26/2010 Khorfakkan Hospital Pediatric Department 3
  4. 4. Fifteen to 20% of infants with hypoxic-ischemic encephalopathy die in the neonatalperiod 25-30% of survivors are left with permanent neurodevelopmental abnormalities (cerebral palsy, mental retardation). Dixon G, Badawi N, Kurinczuk JJ, et al: Early developmental outcomes after newborn encephalopathy. Pediatrics 2002;109:26-3305/26/2010 Khorfakkan Hospital Pediatric Department 4
  5. 5. Effects of Asphyxia System Effect I. Central nervous system II.Cardiovascular 1.Hypoxic-ischemic encephalopathy 1.Myocardial ischemia 2.Infarction 2. Poor contractility 3. Intracranial hemorrhage 3. Cardiac stun 4.Seizures 4. Tricuspid insufficiency 5. Cerebral edema 5. Hypotension 6. Hypotonia 7. Hypertonia Cowan F, Rutherford M, Groenendaal F, et al: Origin and timing of brain lesions in term infants with neonatal encephalopathy. Lancet 2003;361:736- 42.05/26/2010 Khorfakkan Hospital Pediatric Department 5
  6. 6. Effects of Asphyxia System Effect (cont.) III. Pulmonary V. Adrenal 1. Pulmonary hypertension Adrenal hemorrhage 2. Pulmonary hemorrhage 3. Respiratory distress syndrome VI. Gastrointestinal 1. Perforation IV. Renal 2. Ulceration with hemorrhage Acute tubular or cortical necrosis 3. Necrosis Cowan F, Rutherford M, Groenendaal F, et al: Origin and timing of brain lesions in term infants with neonatal encephalopathy. Lancet 2003;361:736- 42.05/26/2010 Khorfakkan Hospital Pediatric Department 6
  7. 7. Effects of Asphyxia System Effect (cont.)VII. Metabolic1. Inappropriate secretion of antidiuretic hormone2. Hyponatremia3. Hypoglycemia VIII. Integument4. Hypocalcemia Subcutaneous fat necrosis5. Myoglobinuria IX. Hematology Disseminated intravascular coagulation Cowan F, Rutherford M, Groenendaal F, et al: Origin and timing of brain lesions in term infants with neonatal encephalopathy. Lancet 2003;361:736- 42. 05/26/2010 Khorfakkan Hospital Pediatric Department 7
  8. 8. Asphyxia is considered in infants with: 1. Fetal acidosis (pH <7.0) 2. A 5-min Apgar score of 0-3 3. Hypoxic-ischemic encephalopathy: i. Altered tone ii. Depressed level of consciousness iii. Seizures And 4. Other multiorgan system signs Battin MR, Dezoete A, Gunn TR, et al: Neurodevelopmental outcome of infants treated with head cooling and mild hypothermia after perinatal asphyxia. Pediatrics 2001;107:48005/26/2010 Khorfakkan Hospital Pediatric Department 8
  9. 9. Causes Of Fetal Hypoxia (1) Inadequate oxygenation of maternal blood as a result of: I. Hypoventilation during anesthesia II. Cyanotic heart disease III. Respiratory failure IV. Carbon monoxide poisoning (2) low maternal blood pressure as a result of the hypotension that may: I. Complicate spinal anesthesia II. Result from compression of the vena cava and aorta by the gravid uterus05/26/2010 Khorfakkan Hospital Pediatric Department 9
  10. 10. Causes Of Fetal Hypoxia (cont.) (3) Inadequate relaxation of the uterus to permit placental filling as a result of uterine tetany caused by the administration of excessive oxytocin (4) Premature separation of the placenta Johnson MV: MRI for neonatal encephalopathy in full-term infants. Lancet 2003;361:713-405/26/2010 Khorfakkan Hospital Pediatric Department 10
  11. 11. Causes Of Fetal Hypoxia (cont.) (5) Impedance to the circulation of blood through the umbilical cord as a result of compression or knotting of the cord (6) Uterine vessel vasoconstriction by cocaine (7) placental insufficiency from numerous causes including toxemia and postmaturity. Johnson MV: MRI for neonatal encephalopathy in full-term infants. Lancet 2003;361:713-405/26/2010 Khorfakkan Hospital Pediatric Department 11
  12. 12. Fetal hypoxia Abnormal Doppler velocimetry . On an umbilical artery Doppler flow velocity waveform The umbilical placental impedance is so high that the diastolic component shows flow in a reverse direction. This finding is an indication of severe intrauterine hypoxia and intrauterine growth restriction . Nelson Textbook of Pediatrics (on 20 November 2003) 2003 Elsevier05/26/2010 Khorfakkan Hospital Pediatric Department 12
  13. 13. Causes of after birth hypoxia (1)Anemia severe enough to lower the oxygen content of the blood to a critical level, as after severe hemorrhage or hemolytic disease (2) Shock severe enough to interfere with the transport of oxygen to vital organs as a result of i. Overwhelming infection ii. Massive blood loss iii. Intracranial or adrenal hemorrhage Crowley P: Prophylactic corticosteroids for preterm birth. Cochrane Database Syst Rev 2002;Issue 1. De Felice C, Toti P, Laurini RN, et al: Early neonatal brain injury in histologic chorioamnionitis. J Pediatr05/26/2010 Khorfakkan Hospital Pediatric Department2001;138:101 13
  14. 14. Causes of after birth hypoxia (cont.) (3) Deficit in arterial oxygen saturation from failure to breathe adequately postnatally because of i. Cerebral defect ii. Narcosis iii. Injury(4) Failure of oxygenation of an adequate amountof blood as a result of severe forms of cyanotic congenital heart disease orpulmonary disease Crowley P: Prophylactic corticosteroids for preterm birth. Cochrane Database Syst Rev 2002;Issue 1. De Felice C, Toti P, Laurini RN, et al: Early neonatal brain injury in histologic chorioamnionitis. J Pediatr 2001;138:10105/26/2010 Khorfakkan Hospital Pediatric Department 14
  15. 15. PathophysiologyWithin minutes of the onset of total fetal hypoxia : 1.Bradycardia 2. Hypotension 3. decreased cardiac output 4. severe metabolic as well as respiratory acidosis occur The initial circulatory response of the fetus * is increased shunting through the ductus venosus, ductus arteriosus, and foramen ovale * with transient maintenance of perfusion of the brain, heart, and adrenals in preference to the lungs (because of pulmonary vasoconstriction), liver, kidneys, and intestine.05/26/2010 Khorfakkan Hospital Pediatric Department 15
  16. 16. Patterns of periodic fetal heart rate (FHR)deceleration A shows early deceleration occurring during the peak of uterine contractions as a result of pressure on the fetal head . Hon EH: An Atlas of Fetal Heart Rate Patterns . New Haven, CT, Harty Press, 1968.) 05/26/2010 Khorfakkan Hospital Pediatric Department 16
  17. 17. Patterns of periodic fetal heart rate(FHR) deceleration (cont . ) B, Late deceleration caused by uteroplacental insufficiency . Hon EH: An Atlas of Fetal Heart Rate Patterns . New Haven, CT, Harty Press, 1968.) 05/26/2010 Khorfakkan Hospital Pediatric Department 17
  18. 18. Patterns of periodic fetal heart rate(FHR) deceleration (cont.) C, Variable deceleration as a result of umbilical cord compression . Hon EH: An Atlas of Fetal Heart Rate Patterns . New Haven, CT, Harty Press, 1968.) 05/26/2010 Khorfakkan Hospital Pediatric Department 18
  19. 19. Clinical Manifestations Hypoxic-Ischemic Encephalopathy in Term Infants Signs: Stage 1 Stage 2 Stage 3 I. Level of consciousness Hyperalert , Lethargic Stuporous coma II. Muscle tone Normal Hypotonic Flaccid III. Posture Normal Flexion Decerebrate Biagioni E, Mercuri E, Rutherford M, et al: Combined use of electroencephalogram and magnetic resonance imaging in full-term neonates with acute encephalopathy. Pediatrics 2001;107:46105/26/2010 Khorfakkan Hospital Pediatric Department 19
  20. 20. Clinical Manifestations Hypoxic-Ischemic Encephalopathy in Term Infants (cont.) Signs: Stage 1 Stage 2 Stage 3 IV. Tendon reflexes Clonus ,Hyperactive Hyperactive Absent V. Myoclonus Present Present Absent VI. Moro reflex Strong Weak Absent Biagioni E, Mercuri E, Rutherford M, et al: Combined use of electroencephalogram and magnetic resonance imaging in full-term neonates with acute encephalopathy. Pediatrics 2001;107:46105/26/2010 Khorfakkan Hospital Pediatric Department 20
  21. 21. Clinical Manifestations Hypoxic-Ischemic Encephalopathy in Term Infants (cont.) Signs: Stage 1 Stage 2 Stage 3 VII. Pupils Mydriasis Miosis Unequal Poor light reflex VIII. Seizures None Common Decerebration IX. Electroencephalographic Normal Low voltage changing Burst suppression to seizure activity Rutherford M, etto isoelectric of Biagioni E, Mercuri E, al: Combined use electroencephalogram and magnetic resonance imaging in full-term neonates with acute encephalopathy. Pediatrics 2001;107:46105/26/2010 Khorfakkan Hospital Pediatric Department 21
  22. 22. Clinical Manifestations Hypoxic-Ischemic Encephalopathy in Term Infants (cont.) Signs: Stage 1 Stage 2 Stage 3 X. Duration <24 hr if progresses; otherwise, Days to weeks may remain normal24 hr to 14 days XI. Outcome Good Variable Death, severe deficits Biagioni E, Mercuri E, Rutherford M, et al: Combined use of electroencephalogram and magnetic resonance imaging in full-term neonates with acute encephalopathy. Pediatrics 2001;107:46105/26/2010 Khorfakkan Hospital Pediatric Department 22
  23. 23. Treatment Therapy is supportive and directed at the organ system manifestations Careful attention to : • Ventilatory status and adequate oxygenation • Blood volume, • Hemodynamic status • Acid-base balance • Possible infection is important Dixon G, Badawi N, Kurinczuk JJ, et al: Early developmental outcomes after newborn encephalopathy. Pediatrics 2002;109:26-33.05/26/2010 Khorfakkan Hospital Pediatric Department 23
  24. 24. Treatment (cont.) No established effective treatment is available for the brain tissue injury, although many drugs (phenobarbital, allopurinol, calcium channel blockers) and procedures (total body or local cranial hypothermia) are under study Aggressive treatment of seizures is critical and may necessitate continuous electroencephalographic monitoring. Dixon G, Badawi N, Kurinczuk JJ, et al: Early developmental outcomes after newborn encephalopathy. Pediatrics 2002;109:26-33.05/26/2010 Khorfakkan Hospital Pediatric Department 24
  25. 25. Treatment (cont.) Seizure activity may be severe and refractory to the usual doses of anticonvulsants Phenobarbital, the drug of choice, is given with an intravenous loading dose (20 mg/kg); additional doses of 10 mg/kg (up to 40-50 mg/kg total) may be needed. Phenobarbital levels should be monitored 24 hr after the loading dose and maintenance therapy (5 mg/kg/24 hr) are begun Phenytoin (20 mg/kg loading dose) or lorazepam (0.1 mg/kg) may be needed for refractory seizures. Dixon G, Badawi N, Kurinczuk JJ, et al: Early developmental outcomes after newborn encephalopathy. Pediatrics 2002;109:26-33.05/26/2010 Khorfakkan Hospital Pediatric Department 25
  26. 26. Prognosis The outcome of hypoxic-ischemic encephalopathy ranges from complete recovery to death The prognosis depending on : 1.Whether the metabolic and cardiopulmonary complications (hypoxia, hypoglycemia, shock) can be treated 2. Infants gestational age (outcome is poorest if the infant is preterm) 3. Severity of the encephalopathy Battin MR, Dezoete A, Gunn TR, et al: Neurodevelopmental outcome of infants treated with head cooling and mild hypothermia after perinatal asphyxia. Pediatrics 2001;107:480.05/26/2010 Khorfakkan Hospital Pediatric Department 26
  27. 27. Prognosis (Cont.) Severe encephalopathy characterized by : 1.Flaccid coma 2.Apnea 3.Absence oculocephalic reflexes 4. Refractory seizures Is associated with a poor prognosis Battin MR, Dezoete A, Gunn TR, et al: Neurodevelopmental outcome of infants treated with head cooling and mild hypothermia after perinatal asphyxia. Pediatrics 2001;107:480.05/26/2010 Khorfakkan Hospital Pediatric Department 27
  28. 28. Prognosis (Cont.) 1. A low Apgar score at 20 min 2. Absence of spontaneous respirations at 20 min of age 3. Persistence of abnormal neurologic signs at 2 wk of age predict death or severe cognitive and motor deficits Battin MR, Dezoete A, Gunn TR, et al: Neurodevelopmental outcome of infants treated with head cooling and mild hypothermia after perinatal asphyxia. Pediatrics 2001;107:480.05/26/2010 Khorfakkan Hospital Pediatric Department 28
  29. 29. Prognosis (Cont.)Brain death after neonatal hypoxic-ischemic encephalopathy is diagnosed by: 1. Clinical findings of coma unresponsive to pain, auditory, or visual stimulation 2. Apnea with Pco2 rising from 40 to over 60 mm Hg 3. Absent brainstem reflexes (pupil, oculocephalic, oculovestibular, corneal, gag, sucking) Battin MR, Dezoete A, Gunn TR, et al: Neurodevelopmental outcome of infants treated with head cooling and mild hypothermia after perinatal asphyxia. Pediatrics 2001;107:480.05/26/2010 Khorfakkan Hospital Pediatric Department 29
  30. 30. Thank you05/26/2010 Khorfakkan Hospital Pediatric Department 30

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