Perinatal asphyxia

16,958 views

Published on

Published in: Health & Medicine
0 Comments
30 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
16,958
On SlideShare
0
From Embeds
0
Number of Embeds
17
Actions
Shares
0
Downloads
1,094
Comments
0
Likes
30
Embeds 0
No embeds

No notes for slide

Perinatal asphyxia

  1. 1. PERINATAL ASPHYXIA –PATHOPHYSIOLOGYICAL PARADOX AND RECENT TRENDS IN MANAGEMENT Dr Varsha Atul shah
  2. 2. PERINATAL ASPHYXIAq Insult to the fetus / Newborn ± Lack of oxygen (Hypoxia) ± Lack of perfusion (Ischemia)q Effect of hypoxia & Ischemia inseperableq Both contribute to tissue injury
  3. 3. ESSENTIAL CRITERIA FOR PERINATAL ASPHYXIAq Prolonged metabolic or mixed acidemia (pH < 7.00) on an umbilical cord arterial blood sampleq Persistence of an Apgar score of 0-3 for > 5 minutesq Clinical neurological manifestations e.g. seizure, hypotonia, coma or hypoxic-ischaemic encephalopathy in the immediate neonatal periodq Evidence of multiorgan system dysfunction in the immediate neonatal periods
  4. 4. PERINATAL ASPHYXIA Western India Scenario (NNF data Base)Incidence 1 – 1.5 / 1000 10%Cause of Perinatal death 20% 26%Still Birth + P. Mort. 50% 59%
  5. 5. ETIOLOGYq Intrapartum or Antepartum (90%) ± Placental Insufficiencyq Post partum (10%) ± Pulmonary ± Cardiovascular ± Neurologic Insufficiency
  6. 6. FACTORS ↓ Mat. Oxygenation↑ Fetal O2 Req. ↓ Blood flow mother to placenta↓ Gas Exchangeacross placenta ↓ Blood flowor fetal tissue placenta to fetus
  7. 7. PATHOPHYSIOLOGY Hypoxia Diving seal reflexShunting of blood Away fromto brain adrenals lungs, kidney& heart gut & skin NON BRAIN ORGAN INJURY
  8. 8. PATHOPHYSIOLOGY Asphyxia continues Shunting within the brain Anterior PosteriorCirculation Circulation Suffers Maintained CEREBRAL CORTICAL LESIONS
  9. 9. PATHOPHYSIOLOGY q Near total asphyxia ± Cord accidents ± Maternal CP arrest q Hypoxia – ABRUPT & SEVERE ± No time for compensationTHALAMUS & BRAIN STEM INJURY, CORTEX SPARED
  10. 10. PATHOLOGYq Target organs of perinatal asphyxia ± Kidneys 50% ± Brain 28% ± Heart 25% ± Lung 23% ± Liver, Bowel, Bone marrow < 5%
  11. 11. NEUROPATHOLOGICAL CHANGESPattern seen in term babiesq Selective neuronal necrosis (Spastic CP)q Status Marmoratus (Chorea, Athetoid, Dystonia)q Parasagittal cerebral injury (Prox Spastic Quadriparesis)q Focal and multifocal ischemic brain injury (sp. Hemiparesis, cognitive defects, seizure)Pattern predominant in pretermq Periventricular leukomalacia
  12. 12. PATHOLOGY At cellular level Cerebral O2 ↓ Substrate supply ↓Synaptic inactivation (Reversible) Further ↓ in perfusion Energy failure Memb. pump failure
  13. 13. ISCHEMIA-RELATED GENERATION OF HYPOXANTHINE I ATP ↓ S ↓ C AMP ↓ H ↓ Adenosine E ↓ ↓ M Inosine I ↓ ↓ A Hypoxanthine
  14. 14. ISCHEMIA AND REPERFUSION INJURYIschemia ATP Calcium influx depletion Phospholipase activation Arachidonic acid release Prostaglandins Proteases, lipases Vasodilation Microvascular Reperfusion permeability ROS Release
  15. 15. MECHANISM RESUSCITATION ATP ASPHYXIA Oxygen HYPOXANTHINEOxygen free radicals BLOCKED XANTHINE Oxygen BLOCKEDOxygen free radicals URIC ACID
  16. 16. FREE RADICALq Unpairedq Highly reactive
  17. 17. EFFECT OF ROS ROSDNA strand Lipid Neutrophil accumulation breakage peroxidation Release ofMembrane PMN proteases, damage plugging of myeloperoxidase, capillaries prostaglandins Phagocytosis Cell death Ischemia Tissue damage
  18. 18. HIE ↑ Glutamate release NMDA receptor NeurotoxicCa Accumulation In neuronesNeurtoxicity in HIE
  19. 19. CLINICAL MANIFESTATIONS OF HIE q Altered consciousness q Tone problems q Seizure activity q Autonomic disturbances q Abnormalities of peripheral and stem reflexes
  20. 20. CLASSIFICATION OF HIE (LEVENE) Feature Mild Moderate SevereConsciousness Irritable Lethargy ComatoseTone Hypotonia Marked SevereSeizure No Yes ProlongedSucking / Resp. Poor Suck Unable to Unable to suck sustain spont. Resp.
  21. 21. SPECIFIC MANAGEMENT PREVENT FURTHER BRAIN DAMAGEq Maintain temperature, perfusion, oxygenation & ventilationq Correct & maintain normal metabolic & acid base milieuq Prompt management of complications
  22. 22. SUMMARY OF INITIAL MANAGEMENTq Admit in newborn unitq Maintenance of tempq Check vital signsq Check hematocrit, sugar, ABG, electrolyteq I.V lineq Consider vol. expanderq Vit K, stomach wash, urine vol
  23. 23. SUPPORTIVE CAREq TABCFMFMCFq T - Temperatureq A - Airwayq B - Breathingq C - Circulationq F - Fluidq M - Medicationsq F - Feedq M - Monitoringq C - Communicationq F - Followup
  24. 24. SUBSEQUENT MANAGEMENT q Oxygenation & ventilation q Adequate perfusion q Normal glucose & calcium q Normal hematocrit q Treat seizure
  25. 25. TREATMENT OF SEIZURESq Correction of hypoglycemia, hypocalcemia & electrolyteq Prophylactic Phenobarbitone ?q Therapeutic Phenobarbitone 20 mg / kg (loading), 5 mg / kg / d (maintenance)q Lorazepam – 0.05 – 0.1 mg / kgq Diazepam to be avoided
  26. 26. CEREBRAL OEDEMAq Avoid fluid overload (SIADH, ATN)q 30° Head raiseq Maintain PaCo2 25-30mm Hg in ventilated infantsq Mannitol 20% (0.5 - 1g / kg) 6 hrly. x 24 hrs.q Frusemide 1.0 mg / kg every 12 hrs.
  27. 27. PERFUSION CFT derangedq Maintain MAP to maintain CBFq Maintain CVP 5-8mm Hg – Term 3-5mm Hg – Pretermq Avoid Fluid, Colloid & SBC Bolusesq Replace volume slowly
  28. 28. SUPPORTIVE CARE (RECENT ADVANCES)q Role of Mannitol, Steriod & Hyperglycemia ??q Regulatory gene (Regulon)q Hypothermiaq Pentoxifyllineq Enhancement of natural defence - Neurotrophic factor & fibroblast growth factor
  29. 29. POTENTIAL THERAPEUTIC STRATEGIES Approach Target CompoundsBlockade of free- Xanthine oxidase Allopurinol; Oxypurinol radical generation inhibitorsScavenging of Antioxidant SOD, Catalase, oxidants after enzymes Glutathione, generation N-Acetylcysteine Radical scavengers DMSO, DMTU, 21- AminosteroidsBlocking chain α-Tocopherol propagation of secondary oxidantsSubstrate Iron Deferoxamine; manipulation Calcium calcium blockers Glucose ?Increase glucose stores (Contd…)
  30. 30. POTENTIAL THERAPEUTIC STRATEGIES Approach Target CompoundsBlockade of secondary PAF PAF antagonists metabolites or Phospholipases Phospholipase inflammatory mediators inhibitors (quinacrine, hydrocortisone) Neutrophils Selection blockers Reduce activation Block adhesionBlockade of coagulation Block platelet PAF receptor blockers effects adhesionInhibition of excitatory Glutamate receptor Magnesium; MK 801 amino acidsEnhancing endogenous (NMDA) antioxidant capability antagonists Regulon regulation
  31. 31. PREDICTORS OF POOR NEURO DEVELOPMENTAL OUTCOMEq Failure to establish respiration by 5 minutesq Apgar 3 or less in 5 mtsq Onset of Seizure in 12 hrsq Refractory convulsionq Stage III HIEq Inability to establish oral feed by 1 wkq Abnormal EEG & failure to normalise by 7 days of lifeq Abnormal CT, MRI, MR spectroscopy in neonatal period
  32. 32. HIE OUTCOME (METAANALYSIS) Severe Moderate MildRisk of Death 61% 5.6% < 1%Risk of Severe 72% 20% < 1%disability
  33. 33. FUTURE DIRECTIONSq No single magic bullet agentq Multitier combination therapies
  34. 34. & THE FINAL R… RELAX Thank you

×