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Perinatal Asphyxia

Perinatal Asphyxia. Dr Asgar Dudhbhai, MD. MARKERS OF PERINATAL ASPHYXIA. Cord Arterial pH < 7.00 Apgar score < 3 for longer than 5 minutes Base Deficit >14 Neonatal encephalopathy (seizures, coma, hypotonia) Multiorgan system dysfunction AAP & ACOG Criteria (1992).

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Perinatal Asphyxia

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  1. Perinatal Asphyxia Dr Asgar Dudhbhai, MD

  2. MARKERS OF PERINATAL ASPHYXIA • Cord Arterial pH < 7.00 • Apgar score < 3 for longer than 5 minutes • Base Deficit >14 • Neonatal encephalopathy (seizures, coma, hypotonia) • Multiorgan system dysfunction AAP & ACOG Criteria (1992)

  3. Perlman JM – Pediatrics 1997;99(6):851-9

  4. Perlman JM – Pediatrics 1997;99(6):851-9

  5. PATHOPHYSIOLOGY OF ASPHYXIA Perlman JM – Pediatrics 1997;99(6):851-9

  6. INTRAUTERINE reduction or cessation of placental gas exchange. places infant at high risk for perinatal asphyxia secondary to respiratory and CNS depression and cardiac compromise. PERINATAL failure of the newborn infant to establish adequate alveolar ventilation at birth with subsequent hypoxemia and respiratory and metabolic acidosis. ASPHYXIA

  7. Organ system involvement (Piazza AJ – Clin Perinatol 1999;26:749-65)

  8. Morin FC: Response of the fetus circulation to stress – in Polin & Fox (1996)

  9. Multisystem involvement in hypoxic-ischemic insult (cont.) (Piazza AJ – Clin Perinatol 1999;26:749-65)

  10. Multisystem involvement in hypoxic-ischemic insult (Piazza AJ – Clin Perinatol 1999;26:749-65)

  11. TIMING OF HIEHill and Volpe, 1989 30% Intrapartum 20% Antepartum 10% Postpartum 35% Antepartum/ Intrapartum

  12. Insults e.g. Asphyxia Impaired perfusion Opportunity for neuronal rescue Primary neuronal death Delayed neuronal death Cytotoxic mechanisms

  13. Johnston MV et al. - Semin Neonatol 2000;5:75-86

  14. Johnston MV et al. - Semin Neonatol 2000;5:75-86

  15. HIE • Single largest contributor to perinatal mortality • mortality 2-20x in PT infants • mortality 200x in Term infants

  16. Clinical Presentation of HIEFour possible scenarios • There may be no problems either antepartum, during labor, or in the neonatal period • No antepartum problems; however, intrapartum problems may be encountered such as MSAF, FHR abnormalities, but these may be followed by a normal neonatal course • No antepartum problems, (+) signs of intrapartum distress (MSAF, need for resuscitation, low Apgar score), & the infant exhibit clinical s/s of HIE such as seizures, systemic organ injury in the early neonatal period • All 3 scenarios may be preceded by known events associated with antenatal brain injury Scenario 1 & 2 -----> (+) neurological signs by the end of the 1st year of life

  17. HIEDiagnosis • Detail history including placental findings • maternal dis causing uteroplacental insufficiency, electronic fetal monitoring, cord pH, meconium • Physical examination including thorough Neurological exam • EEG and ? other electrical responses • Neuro-imaging studies

  18. HIE Sarnat Staging • Birth to 12 hrs • stupor or coma • periodic breathing or resp failure • intact brainstem responses • hypotonia w/paucity of movements • seizure (Sz)

  19. HIE Area of Brain injured Neurological sign • Bilateral cortices or Stupor coma reticular activating system • Cortex, + thalamus Seizures or brainstem • Hypothalamus SIADH • Cerebral/cerebellar Hypotonia cortex, ant horn cell

  20. HIE Sarnat Staging • 12-24 hrs of life • seeming increase in “alertness” • continued Sz activity • apnea • jitteriness • weakness-patterns depend on GA

  21. HIE Sarnat Staging • 24-72 hrs of life • relapse into coma • resp arrest if not assisted • brainstem responses impaired or lost • signs of increasing ICP • signs depends on GA (premies: IVH, term: cerebral necrosis)

  22. HIE Sarnat Staging • >72 hrs of life • coma resolves slowly • tone becomes increased, weakness obvious • disturbed lower brainstem reflexes • sucking, swallowing, tongue movements, gag

  23. Inder TE & Volpe JJ Semin Neonatol 2000;5:3-16

  24. Neuropathology of Hypoxic-Ischemic Cerebral Injury cont.

  25. Neuropathology of Hypoxic-Ischemic Cerebral Injury

  26. Clinical Presentation of HIEFour possible scenarios • There may be no problems either antepartum, during labor, or in the neonatal period • No antepartum problems; however, intrapartum problems may be encountered such as MSAF, FHR abnormalities, but these may be followed by a normal neonatal course • No antepartum problems, (+) signs of intrapartum distress (MSAF, need for resuscitation, low Apgar score), & the infant exhibit clinical s/s of HIE such as seizures, systemic organ injury in the early neonatal period • All 3 scenarios may be preceded by known events associated with antenatal brain injury Scenario 1 & 2 -----> (+) neurological signs by the end of the 1st year of life

  27. Rivkin MJ – Clin Perinatol 1997;24:607-25

  28. Poucyrous M – Clin Perinatol 1999;26:811-28

  29. (Rivkin MJ – Clin Perinatol 1997;24:607-25)

  30. Hypoxic-ischemic brain injury in the term newborn(Rivkin MJ – Clin Perinatol 1997;24:607)

  31. Hypoxic-ischemic brain injury in the term newborn(Rivkin MJ – Clin Perinatol 1997;24:607)

  32. Perlman JM – Pediatrics 1997;99(6):851-9

  33. Tan & Parks –Clin Perinatol 1999;26:733-47

  34. Tan & Parks –Clin Perinatol 1999;26:733-47

  35. Tan & Parks –Clin Perinatol 1999;26:733-47

  36. PRESENTLY APPROVED Allopurinol Ascorbic acid Vitamin E Magnesium sulfate Flunarizine Nimodipine Phenobarbital EXPERIMENTAL Monosialogangliosides -Lipoic acid and dihydrolipoic acid Nitric oxide synthase (NOS) inhibitors Excitatory amino acid antagonists Brain hypothermia Nerve growth factors Interventional strategies based on clinical availability (Tan & Parks – Clin Perinatol 1999;26:733-47)

  37. Agents Tested in Human Subjects

  38. Agents Tested in Human Subjects(continued)

  39. Agents Tested in Human Subjects(continued)

  40. Therapeutic Issues and Limitations • Most concepts of hypoxic-ischemic brain injury are derived from adult models of stroke. (unilateral) • Development of brain function is an important factor in the manifestation of brain injury. (variable cell susceptibility; drug penetration) • Timing of insult is important in relation to delivery of the fetus and initiation of treatment. (therapeutic window; dosage) • The clinical endpoint of asphyxia does not readily translate into a definitive syndrome of brain injury. (biomarkers of brain injury) • A long latent period is necessary for clinical manifestations of brain deficits. • Differential endpoints are used in animal and clinical studies. (adverse drug effects)

  41. Potentially Useful Modalities for Timing Injury Antenatal Modalities Ultrasound Fetal Heart Rate Tracings Intrapartum Modalities Fetal Heart Rate Tracings Nucleated Red Blood Cells Fetal acid/base status Neonatal Modalities Ultrasound CT Scan MRI EEG

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