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