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Hypoxic ischemic encephalopathy

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Matt Kimolo

HIE has been one of the problems facing newborns due to birth asphyxia caused by variety of conditions during child birth or after childbirth, i hope the readers will learn something from the slides

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Dr. Mathias A. Kimolo, MD
? The HIE refers to the characteristic neurological manifestations in term and near-term newborns which develops soon after birth following perinatal asphyxia, it is characterized by clinical and laboratory evidence of acute or sub acute brain injury. ? The primary causes of this condition are systemic hypoxemia and/or reduced cerebral blood flow (CBF) ? Birth asphyxia causes 23% of all neonatal deaths worldwide ? incidence: 3-5 per 1000 full-term live births. ? Half of them progress to moderate to severe HIE
? Birth asphyxia is the cause of 23% of all neonatal deaths worldwide. ? It is one of the top 20 leading causes of burden of disease in all age groups (in terms of disability life adjusted years) by WHO and is the fifth largest cause of death of children younger than 5 years(8%). ? Birth asphyxia is estimated to account for 920,000 neonatal deaths every year and is associated with another 1.1 million intrapartum stillbirths. ? More than a million children who survive birth asphyxia develop problems such as CP, mental retardation, learning difficulties and other disabilities.
Hypoxic ischemic encephalopathy
Pathophysiology of hypoxic-ischemic brain injury in the developing brain. During the initial phase of energy failure, glutamate mediated excitotoxicity and Na+/K+ ATPase failure lead to necrotic cell death. After transient recovery of cerebral energy metabolism, a secondary phase of apoptotic neuronal death occurs. ROS=Reactive Oxygen Species
? Antepartum -placental insufficiency -impaired maternal 02 -decreased blood flow from mother to placenta -decreased bf from placenta to fetus -impaired gas exchange across placenta or fetal tissues -increased fetal o2 requirements (anemia, infection or IUGR) ? Intrapartum, and -Oxygenation failure ( fetal cyanotic CHD, severe pulmonary distress) -Severe anemia (severe hemorrhage, Hemolytic disease) -shock ? Postpartum period. -No breathing or DIB at birth.
? Clinical features and prognosis are based on the severity of the HIE in which there is; >Mild HIE >Moderate HIE, and >Severe HIE.
Hypoxic ischemic encephalopathy
? Seizures are usually generalized and their frequency may increase during the 24-48 hours after onset correlating with the phase of reperfusion injury ? Depressed deep tendon reflexes (DTR) + generalized hypotonia is common ? Ocular motions disturbances, such as skewed deviation of eyes, nystagmus, bobbing and loss of ¡°doll¡¯s eye¡± (ie, conjugate) movements may be revealed by CN examination ? Pupils may be dilated, fixed, or poorly reactive to light.
? Guidelines from American Academy of Pediatrics (AAP) and the American College of Obstetrics and Gynecology (ACOG) for HIE indicate that all of the following must be present for the designation of perinatal asphyxia severe enough to result in acute neurologic injury: 1. Profound metabolic or mixed acidemia (pH<7) in an umbilical artery BS, if obtained 2. Persistence of an Apgar score of 0-3 for longer than 5min 3. Neonatal neurologic sequelae (eg, seizures, coma, hypotonia) 4. Multiple organ involvements (eg, kidney, lungs, liver, heart, intestines)
? INVESTIGATIONS ? There are 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 the systemic organs LABORATORY STUDIES ? Serum electrolyte levels ? Renal function studies ? Cardiac enzymes and LFTs- to assess the degree of hypoxic-ischemic injury to heart and liver ? Coagulation profile (PT, PTT and fibrinogen levels) ? Arterial blood gases- to asses acid-base status and to avoid hyperoxia and hypoxia, as well as hypercapnia and hypocapnia
? IMAGING STUDIES -MRI -Cranial ultrasound -Echocardiography ? ADDITIONAL STUDIES -EEG -Hearing test- an increased incidence of deafness has been found among infants with HIE who require assisted ventilation -retinal and ophthalmic examination
Goal of Treatment ?Maintain TABC, ?Optimize Cardiac Output and Cerebral Perfusion, ?Maintain SpO2 ?Treat/Prevent Hypoglycemia
? Supportive therapy, ? Anticonvulsants, ? Cerebroprotective interventions, and ? Monitoring.
? IV fluid *10%dextrose ? Treat hypotension; dobutamine, and dopamine. ? Temperature; cool therapy(33-34c) ? Calcium levels should be kept in the normal range (9-11mg/dl)
? Control seizures: -phenobarbitone: *Loading dose: 20mg/kg slowly *Maintenance dose: 5mg/kg/day -Phenytoin as a second line drug -Lorazepam *(0.05-0.1mg/kg/dose i.v) for seizures not responding to phenobarbitone and/or phenytoin.
? Therapeutic hypothermia (cool therapy), ? Free radical scavengers, ? Antagonists of excitotoxic amino acids, ? Calcium channel Blockers.
Hypoxic ischemic encephalopathy
? SHORT TERM -Death ? LONG TERM ? Developmental delay ? Cerebral palsy ? Microcephaly ? Seizures ? Blindness ? Deafness ? Problems with cognition, memory, fine motor skills and behavior.
1. Emedicine.Medscape.com 2. https://www.ncbi.nlm.nih.gov

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Hypoxic ischemic encephalopathy

  • 1. Dr. Mathias A. Kimolo, MD
  • 2. ? The HIE refers to the characteristic neurological manifestations in term and near-term newborns which develops soon after birth following perinatal asphyxia, it is characterized by clinical and laboratory evidence of acute or sub acute brain injury. ? The primary causes of this condition are systemic hypoxemia and/or reduced cerebral blood flow (CBF) ? Birth asphyxia causes 23% of all neonatal deaths worldwide ? incidence: 3-5 per 1000 full-term live births. ? Half of them progress to moderate to severe HIE
  • 3. ? Birth asphyxia is the cause of 23% of all neonatal deaths worldwide. ? It is one of the top 20 leading causes of burden of disease in all age groups (in terms of disability life adjusted years) by WHO and is the fifth largest cause of death of children younger than 5 years(8%). ? Birth asphyxia is estimated to account for 920,000 neonatal deaths every year and is associated with another 1.1 million intrapartum stillbirths. ? More than a million children who survive birth asphyxia develop problems such as CP, mental retardation, learning difficulties and other disabilities.
  • 5. Pathophysiology of hypoxic-ischemic brain injury in the developing brain. During the initial phase of energy failure, glutamate mediated excitotoxicity and Na+/K+ ATPase failure lead to necrotic cell death. After transient recovery of cerebral energy metabolism, a secondary phase of apoptotic neuronal death occurs. ROS=Reactive Oxygen Species
  • 6. ? Antepartum -placental insufficiency -impaired maternal 02 -decreased blood flow from mother to placenta -decreased bf from placenta to fetus -impaired gas exchange across placenta or fetal tissues -increased fetal o2 requirements (anemia, infection or IUGR) ? Intrapartum, and -Oxygenation failure ( fetal cyanotic CHD, severe pulmonary distress) -Severe anemia (severe hemorrhage, Hemolytic disease) -shock ? Postpartum period. -No breathing or DIB at birth.
  • 7. ? Clinical features and prognosis are based on the severity of the HIE in which there is; >Mild HIE >Moderate HIE, and >Severe HIE.
  • 9. ? Seizures are usually generalized and their frequency may increase during the 24-48 hours after onset correlating with the phase of reperfusion injury ? Depressed deep tendon reflexes (DTR) + generalized hypotonia is common ? Ocular motions disturbances, such as skewed deviation of eyes, nystagmus, bobbing and loss of ¡°doll¡¯s eye¡± (ie, conjugate) movements may be revealed by CN examination ? Pupils may be dilated, fixed, or poorly reactive to light.
  • 10. ? Guidelines from American Academy of Pediatrics (AAP) and the American College of Obstetrics and Gynecology (ACOG) for HIE indicate that all of the following must be present for the designation of perinatal asphyxia severe enough to result in acute neurologic injury: 1. Profound metabolic or mixed acidemia (pH<7) in an umbilical artery BS, if obtained 2. Persistence of an Apgar score of 0-3 for longer than 5min 3. Neonatal neurologic sequelae (eg, seizures, coma, hypotonia) 4. Multiple organ involvements (eg, kidney, lungs, liver, heart, intestines)
  • 11. ? INVESTIGATIONS ? There are 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 the systemic organs LABORATORY STUDIES ? Serum electrolyte levels ? Renal function studies ? Cardiac enzymes and LFTs- to assess the degree of hypoxic-ischemic injury to heart and liver ? Coagulation profile (PT, PTT and fibrinogen levels) ? Arterial blood gases- to asses acid-base status and to avoid hyperoxia and hypoxia, as well as hypercapnia and hypocapnia
  • 12. ? IMAGING STUDIES -MRI -Cranial ultrasound -Echocardiography ? ADDITIONAL STUDIES -EEG -Hearing test- an increased incidence of deafness has been found among infants with HIE who require assisted ventilation -retinal and ophthalmic examination
  • 13. Goal of Treatment ?Maintain TABC, ?Optimize Cardiac Output and Cerebral Perfusion, ?Maintain SpO2 ?Treat/Prevent Hypoglycemia
  • 14. ? Supportive therapy, ? Anticonvulsants, ? Cerebroprotective interventions, and ? Monitoring.
  • 15. ? IV fluid *10%dextrose ? Treat hypotension; dobutamine, and dopamine. ? Temperature; cool therapy(33-34c) ? Calcium levels should be kept in the normal range (9-11mg/dl)
  • 16. ? Control seizures: -phenobarbitone: *Loading dose: 20mg/kg slowly *Maintenance dose: 5mg/kg/day -Phenytoin as a second line drug -Lorazepam *(0.05-0.1mg/kg/dose i.v) for seizures not responding to phenobarbitone and/or phenytoin.
  • 17. ? Therapeutic hypothermia (cool therapy), ? Free radical scavengers, ? Antagonists of excitotoxic amino acids, ? Calcium channel Blockers.
  • 19. ? SHORT TERM -Death ? LONG TERM ? Developmental delay ? Cerebral palsy ? Microcephaly ? Seizures ? Blindness ? Deafness ? Problems with cognition, memory, fine motor skills and behavior.

Editor's Notes

  • #5: -Diving seal reflex -In human adults BP range for CBF maintenance= 60-100mm hg -In healthy term neonate BP range for CBF autoregulation maintenance= 10-20mm Hg -CBF becomes pressure-passive i.e depends on systemic BP -magnitude of neuronal damage is proportional to the duration and severity of the initial insult combined with effects of reperfusion injury and apoptosis