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PERINATAL ASPHYXIA PATHOPHYSIOLOGYICAL PARADOX AND RECENT TRENDS IN MANAGEMENT

PERINATAL ASPHYXIA. Insult to the fetus / NewbornLack of oxygen (Hypoxia)Lack of perfusion (Ischemia)Effect of hypoxia

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PERINATAL ASPHYXIA PATHOPHYSIOLOGYICAL PARADOX AND RECENT TRENDS IN MANAGEMENT

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    1. PERINATAL ASPHYXIA PATHOPHYSIOLOGYICAL PARADOX AND RECENT TRENDS IN MANAGEMENT Dr. A. K. Dutta Director Prof. & HOD, Pediatrics Kalawati Saran Childrens Hospital Lady Harding Medical College New Delhi

    2. PERINATAL ASPHYXIA Insult to the fetus / Newborn Lack of oxygen (Hypoxia) Lack of perfusion (Ischemia) Effect of hypoxia & Ischemia inseperable Both contribute to tissue injury

    3. ESSENTIAL CRITERIA FOR PERINATAL ASPHYXIA Prolonged metabolic or mixed acidemia (pH < 7.00) on an umbilical cord arterial blood sample Persistence of an Apgar score of 0-3 for > 5 minutes Clinical neurological manifestations e.g. seizure, hypotonia, coma or hypoxic-ischaemic encephalopathy in the immediate neonatal period Evidence of multiorgan system dysfunction in the immediate neonatal periods

    4. PERINATAL ASPHYXIA

    5. ETIOLOGY Intrapartum or Antepartum (90%) Placental Insufficiency Post partum (10%) Pulmonary Cardiovascular Neurologic Insufficiency

    6. FACTORS ? Mat. Oxygenation

    7. PATHOPHYSIOLOGY Hypoxia

    8. PATHOPHYSIOLOGY Asphyxia continues

    9. PATHOPHYSIOLOGY Near total asphyxia Cord accidents Maternal CP arrest Hypoxia ABRUPT & SEVERE No time for compensation

    10. PATHOLOGY Target organs of perinatal asphyxia Kidneys 50% Brain 28% Heart 25% Lung 23% Liver, Bowel, Bone marrow < 5%

    11. NEUROPATHOLOGICAL CHANGES Pattern seen in term babies Selective neuronal necrosis (Spastic CP) Status Marmoratus (Chorea, Athetoid, Dystonia) Parasagittal cerebral injury (Prox Spastic Quadriparesis) Focal and multifocal ischemic brain injury (sp. Hemiparesis, cognitive defects, seizure) Pattern predominant in preterm Periventricular leukomalacia

    12. PATHOLOGY Cerebral O2 ? Substrate supply ? Synaptic inactivation (Reversible) Energy failure Memb. pump failure

    13. ISCHEMIA-RELATED GENERATION OF HYPOXANTHINE I S C H E M I A

    14. ISCHEMIA AND REPERFUSION INJURY Ischemia

    15. MECHANISM RESUSCITATION

    16. FREE RADICAL Unpaired Highly reactive

    17. EFFECT OF ROS ROS

    18. HIE ? Glutamate release

    19. CLINICAL MANIFESTATIONS OF HIE Altered consciousness Tone problems Seizure activity Autonomic disturbances Abnormalities of peripheral and stem reflexes

    20. CLASSIFICATION OF HIE (LEVENE)

    21. SPECIFIC MANAGEMENT PREVENT FURTHER BRAIN DAMAGE Maintain temperature, perfusion, oxygenation & ventilation Correct & maintain normal metabolic & acid base milieu Prompt management of complications

    22. SUMMARY OF INITIAL MANAGEMENT Admit in newborn unit Maintenance of temp Check vital signs Check hematocrit, sugar, ABG, electrolyte I.V line Consider vol. expander Vit K, stomach wash, urine vol

    23. TABCFMFMCF T - Temperature A - Airway B - Breathing C - Circulation F - Fluid M - Medications F - Feed M - Monitoring C - Communication F - Followup SUPPORTIVE CARE

    24. SUBSEQUENT MANAGEMENT Oxygenation & ventilation Adequate perfusion Normal glucose & calcium Normal hematocrit Treat seizure

    25. TREATMENT OF SEIZURES Correction of hypoglycemia, hypocalcemia & electrolyte Prophylactic Phenobarbitone ? Therapeutic Phenobarbitone 20 mg / kg (loading), 5 mg / kg / d (maintenance) Lorazepam 0.05 0.1 mg / kg Diazepam to be avoided

    26. CEREBRAL OEDEMA Avoid fluid overload (SIADH, ATN) 30? Head raise Maintain PaCo2 25-30mm Hg in ventilated infants Mannitol 20% (0.5 - 1g / kg) 6 hrly. x 24 hrs. Frusemide 1.0 mg / kg every 12 hrs.

    27. PERFUSION CFT deranged Maintain MAP to maintain CBF Maintain CVP 5-8mm Hg Term 3-5mm Hg Preterm Avoid Fluid, Colloid & SBC Boluses Replace volume slowly

    28. SUPPORTIVE CARE (RECENT ADVANCES) Role of Mannitol, Steriod & Hyperglycemia ?? Regulatory gene (Regulon) Hypothermia Pentoxifylline Enhancement of natural defence - Neurotrophic factor & fibroblast growth factor

    29. POTENTIAL THERAPEUTIC STRATEGIES

    30. POTENTIAL THERAPEUTIC STRATEGIES

    31. PREDICTORS OF POOR NEURO DEVELOPMENTAL OUTCOME Failure to establish respiration by 5 minutes Apgar 3 or less in 5 mts Onset of Seizure in 12 hrs Refractory convulsion Stage III HIE Inability to establish oral feed by 1 wk Abnormal EEG & failure to normalise by 7 days of life Abnormal CT, MRI, MR spectroscopy in neonatal period

    32. HIE OUTCOME (METAANALYSIS)

    33. FUTURE DIRECTIONS No single magic bullet agent Multitier combination therapies

    36. & THE FINAL R

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