Birth asphyxia

A simple guide to Perinatal Asphyxia and HIE

1. Perinatal Asphyxia & Hypoxic Ischemic Encephalopathy DR. M. S. PRASAD 7/6/2016 1

2. Definitions Anoxia: Complete lack of oxygen. Hypoxia: Decreased availability of oxygen Hypoxemia: Decreased arterial concentration of oxygen. Ischemia: Insufficient blood flow to cells or organ resulting in interrupted metabolism and death of the cell or organ affected. 7/6/2016 2

3. Perinatal Asphyxia (PA) Perinatal asphyxia, neonatal asphyxia, or birth asphyxia is the medical condition resulting from deprivation of oxygen to a newborn infant that causes physical harm, mainly to the brain. 7/6/2016 3

4. Definition The Perinatal Asphyxia may be defined as hypoxic insult to the fetus severe enough to cause metabolic acidosis, neonatal encephalopathy, and multiorgan system dysfunction. 7/6/2016 4

5. Perinatal Asphyxia The NNF of India has defined asphyxia as “gasping or ineffective breathing or lack of breathing at one minute of life” 7/6/2016 5

6. AAP Criteria Umbilical artery blood pH < 7.0. 5 minute apgar score < 3, Neonatal Encephalopathy manifesting as seizures, hypotonia or coma in the immediate neonatal period. Evidence of multiorgan dysfunction. 7/6/2016 6

7. Birth Asphyxia Birth Asphyxia = Perinatal Asphyxia = Neonatal Asphyxia. Incidence: 1 – 6 /1000 live births. 7/6/2016 7

8. Perinatal Asphyxia Perinatal Asphyxia is the leading cause of neonatal death (along with infection, prematurity and LBW). It is the leading cause of neurodevelopmental disability in children. The term perinatal asphyxia is preferred to Birth Asphyxia as asphyxia may occur before, during and after birth. 7/6/2016 8

9. Why it is important? 7/6/2016 9

10. 10 Primary cause of death: NNPD Cause Deaths (n = 1800) Prematurity 27 % Infection 17 % Perinatal hypoxia 29 % Malformation 09 % Other causes 18 % 7/6/2016

11. 11 4 million newborn deaths – Why? almost all are due to preventable conditions 7/6/2016

12. 12 Others: Hypothermia, RD, Jn , Pulm . Haemorrhage , Seizure etc. ICMR 2006 7/6/2016

13. Physiology of Asphyxia When babies become asphyxiated (either in utero or after delivery), they undergo a well defined sequence of events, ie primary apnea followed by secondary apnea. 7/6/2016 13

14. Primary Apnea When an infant is deprived of oxygen, an initial brief period of rapid breathing occurs. If the asphyxia continues, the respiratory movements cease, the HR begins to fall, muscle tone gradually diminishes, and the infant enters a period of apnea known as primary apnea. The initial steps will induce breathing. 7/6/2016 14

15. Secondary Apnea If the asphyxia continues, the infant develops deep gasping respiration, the HR continues to decrease, the BP begins to fall, and the infant becomes nearly flaccid. The respirations become weak and weaker until the infant takes a last gasp and enters a period of apnea called secondary apnea. During secondary apnea the infant does not respond to initial steps. 7/6/2016 15

16. Effects of PA Hypoxic damage to most of the infant's organs (heart, lungs, liver, gut, kidneys), but brain damage is of most concern and perhaps the least likely to heal. In more pronounced cases, an infant will survive, but with damage to the brain manifested as either mental or physical disability, such as developmental delay or intellectual disability, or physical, such as spasticity 7/6/2016 16

17. Effects (continued) Mental Disability: Developmental Delay, Intellectual Disability. Physical Disability: Spasticity, Motor Deficit. Cerebral Palsy. 7/6/2016 17

18. What to do? 7/6/2016 18

19. Routine Care Dry, Provide warmth, Clear airway, if needed, Initiate Breastfeeding, and Monitor Breathing, Heart-Rate and Color. 7/6/2016 19

20. NNR (Neonatal Resuscitation) Initial Steps, Assisted Ventilation, Bag & Mask, Endotracheal Intubation. Chest Compression, Medication. 7/6/2016 20

21. Global Hypoxic Ischemic Insult Global Hypoxic Ischemic Insult of Brain Hypoxic Ischemic Encephalopathy (HIE) 7/6/2016 21

22. Hypoxic-Ischemic Encephalopathy (HIE) The HIE refers to the characteristic neurological manifestations in term and near-term newborns which develop soon after birth following perinatal asphyxia. Incidence: 3-5 per 1000 full-term live births. Half of them progress to moderate to severe HIE. 7/6/2016 22

23. HIE The encephalopathy resulting from hypoxia (low oxygen) and ischemia (low blood flow) mainly to the brain. The HIE refers to the characteristic neurological manifestations in term and near-term newborns which develop soon after birth following perinatal asphyxia. 7/6/2016 23

24. Pathology Lack of adequate breathing  lack of oxygen supply to heart  Inability of heart to pump adequate blood  hypoxia + ischemia to organs (particularly brain). Longer Arrest  Infarct  Brain Death. 7/6/2016 24

25. Brain Regions vulnerable for damage Hippocampus, Purkinje Neurons in Cerebellum, Basal Ganglia, and Brain-stem. 7/6/2016 25

26. Pathogenesis Poorly understood, Hypoxic Ischemic insult can damage periventricular white matter tracks. 7/6/2016 26

27. Etiology Perinatal Asphyxia, Drowning, Airway Obstruction, Trauma, Hanging, Infection 7/6/2016 27

28. Outcome Immediate outcome: Death. Late outcome ( if survived ): Cerebral Palsy, Developmental Delay, Mental Retardation. 7/6/2016 28

29. Further Outcome (complications) Death, Vegetative State, Severe Disability, SIRS, Multiple Organ Dysfunction Syndrome. 7/6/2016 29

30. Etiology of Perinatal Asphyxia Multifactorial, Antepartum: Placental Insufficiency. Intrapartum, and Postpartum period. 7/6/2016 30

31. Placental Insufficiency Impaired maternal oxygenation, Decreased blood flow from the mother to the placenta, Decreased blood flow from placenta to fetus, Impaired gas exchange across placenta or fetal tissues, Increased fetal oxygen requirement. 7/6/2016 31

32. Impaired Maternal Oxygenation Anemia, Pulmonary, or Cardiac, or Neurologic disease in mother. 7/6/2016 32

33. Decreased Blood Flow from the mother to the placenta Maternal Infection, Shock, Dehydration, and Hypotension. 7/6/2016 33

34. Decreased Blood Flow from the Placenta to the Fetus Placental abruption, Cord Prolapse, Cord Entanglement, True Knot, Cord Compression, Abnormality of the umbilical vessels. 7/6/2016 34

35. Impaired Gas Exchange across placenta or fetal tissues Maternal Hypertension, Vascular Disease, Diabetes, Drug Abuse, Post-Maturity, Placental Calcification, infarct or fibrosis. 7/6/2016 35

36. Increased Fetal Oxygen Requirement Fetal Anemia, Fetal Infection, or IUGR 7/6/2016 36

37. Causes Before Birth (Maternal Causes). Inadequate oxygenation of maternal blood. Low Maternal Blood Pressure. At Birth (Fetal or Neonatal Causes). 7/6/2016 37

38. Inadequate Oxygenation of maternal blood Hypoventilation during anesthesia, Cyanotic Heart Disease, Respiratory Failure, CO Poisoning. 7/6/2016 38

39. Low Maternal BP Acute Blood Loss, Spinal Anesthesia, Great Vessels compression by gravid uterus. Uterine Tetany (oxytocin induced) 7/6/2016 39

40. Low Maternal BP (continued) Premature separation of placenta, Compression of knotting of umbilical cord, Placental insufficiency due to toxemia or postmaturity . 7/6/2016 40

41. At Births Failure of oxygenation: Fetal Cyanotic Congenital Heart Disease, Severe Pulmonary Distress. Severe Anemia Severe Hemorrhage, Hemolytic Disease. Shock 7/6/2016 41

42. Shock Sepsis, Massive Blood Loss, Intra-Cranial Hemorrhage, Adrenal Hemorrhage. 7/6/2016 42

43. Pathophysiology 7/6/2016 43

44. Vulnerable Organ Brain, Neonatal Brain has very high requirements for oxygen and baseline blood flow. Hypoxic insult to the fetus initiates diving seal reflex. 7/6/2016 44

45. Diving Seal Reflex Shunting of blood to brain, heart and adrenals and away from lungs, gut, kidneys, liver, spleen and skin, in an attempt to maintain perfusion to more vital organs. 7/6/2016 45

46. Pathophysiology Accumulation of excitatory and toxic amino acids (glutamate) in the damaged tissue. Increased production of free radicals and NO in damaged tissue. 7/6/2016 46

47. Pathophysiology 7/6/2016 47

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49. Biochemical Changes Hypoxia impairs cerebral oxidative metabolism   Increase in lactate,, Fall in pH (acidosis), and Decrease in ATP level. Acidosis   Myocardial Depression   Reduced Cardiac Output. 7/6/2016 49

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53. Brain Damage Term Newborn: Cerebral Cortex, and Basal Ganglia Preterm Newborn: Periventricular White Matter. 7/6/2016 53

54. Circulatory Response of Fetus Increased shunting through Ductus Venosus, Ductus Arteriosus and Foramen Ovale. Inadequate perfusion of periventricular white matter    PVL (periventricular leucomalacia). 7/6/2016 54

55. Causes of Hypotension Myocardial Dysfunction, Capillary Leak Syndrome, and Hypovolemia. 7/6/2016 55

56. Clinical Features 7/6/2016 56

57. Clinical Features Perinatal Asphyxia (no breathing or difficult breathing at birth). IUGR, MSAF (Fetal Distress), Meconium Stained Amniotic Fluid Hypotonic State. 7/6/2016 57

58. Clinical Features Mild HIE, Moderate HIE, and Severe HIE. 7/6/2016 58

59. Mild HIE Transient abnormalities, Poor Feeding, Irritability, or excessive crying, or sleepiness, Slightly increased muscle-tone, Brisk DTR. 7/6/2016 59

60. Moderate HIE Lethargic, Significant hypotonia, Diminished DTR, 7/6/2016 60

61. Moderate HIE (continued) Sluggish or absent Grasp, Moro and Sucking Reflexes. Occasional Apnea, Seizures . 7/6/2016 61

62. Severe HIE Coma, Difficult breathing requiring ventilator support, Decreased Tone, Depressed DTR, Absent neonatal reflexes. 7/6/2016 62

63. Severe HIE (continued) Disturbance of ocular motions, Loss of “doll’s eye” movement, Dilated and fixed pupils with poor LR, Seizures, Full & bulging AF, 7/6/2016 63

64. Investigations No confirmatory laboratory tests to diagnose perinatal asphyxia, Tests are helpful to assess the severity of brain injury and to monitor the functional status of systemic organs. 7/6/2016 64

65. Investigation Blood Sugar, ABG, SpO 2 US in preterm, Serum Electrolytes, Diffuse mediated MRI, CT, aEEG 7/6/2016 65

66. Investigations (continued) Renal Function Tests: Blood Urea, Serum Creatinine. Liver Function Tests, Coagulation Profile PT and PTT. 7/6/2016 66

67. Management 7/6/2016 67

68. Goal of Treatment Maintain TABC, Optimize Cardiac Output and Cerebral Perfusion, Maintain SpO 2 Treat / Prevent Hypoglycemia, 7/6/2016 68

69. Principles of Management Supportive Therapy, Anticonvulsants, Cerebroprotective interventions, and Monitoring. 7/6/2016 69

70. Supportive Therapy IV Fluid: 10% Dextrose, 60 ml/kg/day. Treat Hypotension: Dobutamine , and Dopamine. Temperature: Cool Therapy (33-34 C) 7/6/2016 70

71. Supportive Therapy (continued) Glucose: Treat hypoglycemia, Maintain BS at 75 to 100 mg/dl. Calcium: Calcium level should be kept in the normal range (9 – 11 mg/dl) 7/6/2016 71

72. Anticonvulsants Control Seizures: Phenobarbitone: Loading Dose: 20 mg/kg slowly Maintenance Dose: 5 mg/kg/day Phenytoin as a second line drug Lorazepam (0.05-0.1 mg/kg/dose I. V.) for seizures not responding to Phenobarbitone and/or Phenytoin. 7/6/2016 72

73. Cerebroprotective Interventions Therapeutic Hypothermia (cool therapy), Free Radical Scavengers, Antagonists of excitotoxic amino acids, Calcium Channel Blockers. 7/6/2016 73

74. Caution! Drugs like mannitol, steroids, and furosemide used in past are no longer recommended. 7/6/2016 74

75. Treatment Selective Cerebral or Whole Body Therapeutic Hypothermia (Cool Therapy), Control Seizures, Phenobarbitone/Phenytoin/Midazolam. Mechanical Ventilation, (or ECMO), Volume Expansion, Pressure Amines. 7/6/2016 75

76. Monitoring Regular clinical assessment, Biochemical monitoring, SpO 2 . 7/6/2016 76

77. Clinical Assessment Respiratory Rate, Heart Rate, CRT, BP Temperature, Oxygen Saturation, Urine Output. 7/6/2016 77

78. Prognosis Early Treatment   Better Prognosis. Bad Prognosis: Initial cord or initial blood pH < 6.7, Low Apgar Score (0-3), High Base Deficit, Decrebrate Posture, Lack of spontaneous activity. 7/6/2016 78

79. Mortality Moderate Encephalopathy: 10 to 30% Severe Encephalopathy: Mortality: 60% Disability: 100%. 7/6/2016 79

80. Long Term Handicaps Developmental Delay, Cerebral Palsy, Microcephaly, Seizures Blindness, Deafness, Problems with cognition, memory, fine motor skills and behaviour. 7/6/2016 80

81. Staging of HIE Stage-I Stage-II Stage-III Level of consciousness Hyper-alert Lethargic Stupor/coma Muscle Tone Normal Hypotonic Flaccid Posture Normal Flexion Decerebrate DTR/Clonus Hyperactive Hyperactive Absent Myoclonus Present Present Absent Moro Reflex Strong Weak Absent 7/6/2016 81

82. HIE Staging Stage-I Stage-II Stage-III Pupils Dilated Constricted Unequal Seizures None Common Decerebrate Duration < 24 hrs 24 hrs-14 d Days & Weeks Outcome Good Variable Death or Severe Deficit EEG Normal Low Voltage Bursts 7/6/2016 82