asphyxia.PPT
- 2. PERINATAL ASPHYXIA Insult to the fetus / Newborn Lack of oxygen (Hypoxia) Lack of perfusion (Ischemia) Effect of hypoxia & Ischemia are inseparable Both contribute to tissue injury
- 3. PERINATAL ASPHYXIA There may be associated lactic acidosis If there is hypoventilaiton there may be hypercarbia
- 4. Definition Profound umbilical arterial metabolic or mixed acidemia with PH <7.2 APGAR score of <3 for > 5 minutes Neonatal neurologic sequelae: seizures, hypotonia, coma Multiorgan dysfunction
- 5. PERINATAL ASPHYXIA Western Scenario India Incidence Cause of Perinatal death Still Birth + P. Mort. 1 – 1.5 / 1000 20% 50% 10% 26% 59%
- 6. 12/11/2022 6 4 million newborn deaths – Why? almost all are due to preventable conditions
- 7. 35% 35% 20% 10% During delivery During labor After delivery Before labor
- 8. ETIOLOGY Intrapartum or Antepartum (90%) Placental Insufficiency Cord accident MAS Maternal CP arrest
- 10. ETHIOLOGY I - MATERNAL CAUSES: (conditions leading to imperfect oxygenation of maternal blood) Severe anemia, Hemorrhage & shock, Respiratory failure, and heart failure. Eclamptic seizure, pneumonia, and pulmonary edema.
- 11. ETHIOLOGY II- PLACENTAL CAUSES: Placental compression: interfering with its circulation as in tonically contracted uterus, prolonged labour after rupture of the membranes or as a method of control of bleeding in placenta previa. Placental separation as in accidental hemorrhage. Placental insufficiency e.g. extensive degeneration, multiple infarcts & abnormally small placenta.
- 12. ETHIOLOGY III- CAUSES IN THE UMBILICAL CORD: Obstruction of the circulation, which may be due to: Tight nucal cord True knots Prolapsed cord Compression of the vessels by hematoma of the cord Rupture of vasa praevia.
- 13. ETIOLOGY ( cont…) IV-PROLONGED COMPRESSION OF THE FETAL HEAD: This will cause edema and ischemia, which interfere with the blood supply of the medulla leading to depression of the respiratory center. Prolonged compression may be due to: Contracted pelvis (C/P disproportion). Rigid perineum. Intracranial hemorrhage. Forceps application for a long time. Depressed fracture
- 14. FACTORS Mat. Oxygenation Blood flow mother to placenta Blood flow placenta to fetus Gas Exchange across placenta or fetal tissue Fetal O2 Req.
- 15. Circulatory depression Respiratory depression Hypoxemia Hypercarbia Respiratory acidosis Low cardiac output Decreased tissue perfusion Ischemia Metabolic acidosis Capillary leak, edema Multi-organ dysfunction
- 16. NONE BRAIN ORGAN DAMAGE PATHOPHYSIOLOGY Acute asphyxia Diving reflex Shunting of blood to brain adrenals & heart Away from lungs, kidney gut & skin
- 17. CEREBRAL CORTICAL LESIONS PATHOPHYSIOLOGY Asphyxia continues Shunting within the brain Anterior Circulation Suffers Posterior Circulation Maintained
- 20. THALAMUS & BRAIN STEM INJURY, CORTEX SPARED PATHOPHYSIOLOGY Hypoxia – ABRUPT & SEVERE Complete abruption Cord accident Maternal CP arrest
- 21. Clinical grading OF HIE
- 22. PATHOLOGY Target organs of perinatal asphyxia Kidneys 50% Brain 28% Heart 25% Lung 23% Liver, Bowel, Bone marrow < 5%
- 23. NEUROPATHOLOCIAL CHANGES Pattern seen in term infants 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
- 24. PATHOLOGY Cerebral O2 Substrate supply Synaptic inactivation (Reversible) Energy failure Memb. pump failure Further in perfusion At cellular level
- 26. CHANGES IN SUBSTRATE METABOLISM AND NEURTRANSMITTERS Hypoxic effect Changes that are increased An initial increase Cerebral blood flow Increase of glucose influx to brain Increase in glycogenolysis (increase cAMP) Increase in glycolysis (increase cAMP)
- 27. CHANGES IN SUBSTRATE METABOLISM AND NEURTRANSMITTERS Changed that are decreased Decreased oxidative phosphorylation Eventual decrease brain glucose Decreased phosphocreatinine (PCr) and ATP These changes are more pronouned in the white matter compared to the gray matter
- 28. 12/11/2022 28 GASTROINTESTINAL EFFECTS The asphyxiate infants is at risk for bowel ischemia and NECROTIZING ENTEROCOLITIS
- 29. 12/11/2022 29 HEMATOLOGICS EFFECTS DIC THE LIVER MAY FAIL TO MAKE CLOTTING FACTORS THE BONE MARROW MAY NOT PRODUCE PLATELETS
- 30. 12/11/2022 30 PULMONARY EFFECTS Increased pulmonary resistance pulmonary hemorrhage Pulmonary edema secondary to cardiac failure Failure of surfactant production with secondary HMD Meconium aspiration may be present.
- 31. Management of HIE 1. Maintain O2 and CO2 in normal ranges. 2. Hyperventilation not recommended and may be detrimental. 3. Monitor arterial blood pressure because cerebra perfusion pressure is dependent on MAP 4. Administer volume slowly: overall fluid restriction 5. Monitor electrolytes and glucose 6. Control seizures 7. HYPOTHERMIA THERAPY
- 32. HYPOTHERMIA THERAPY Entry criteria PH < 7.0 Base deficit 16mmole/l in 1st hour APGAR score < 5 at 10 minutes. Less than 6 hrs old. Technique Keep core temp at 33 *C for 72 hrs Continuous EEG monitoring Continue medical management
- 33. MULTISYSTEMIC EFFECTS Seizures Often resitant to anticonvulsant therapy in severe HIE (possibly because of a lack of cortical inhibition Vs. excesive cortical activity 50% are subtle, focal ,multifocal or myoclonic Typically first noted at age 12 to 24 hrs and often resolve by 5 to 7 days Must also assess for other metabolic derangements (eg; hypoglycemia, hypocalcemia, hypomagnesemia) Phenobarbital is the first line agent followed by dilantin (may also consider lorazepam)
- 34. MULTISYSTEMIC EFFECTS ACUTE ASPHYXIA elicits diving reflex with preferred blood flow to the brain, heart, and adrenal gland CARDIAC MANIFESTATIONS Transient myocardial ischemia, congestive heart failure, left or right ventricular dysfunction, tricuspid regurgitation murmur within the first 24 hrs RENAL Oliguria and possible acute tubular necrosis PULMONARY Pulmonary hypertension especially after MAS
- 35. 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 Inability to establish oral feed by 1 wk Abnormal EEG & failure to normalise by 7 days of life Abnormal CT, MRI in neonatal period
- 36. 12/11/2022 36 PREVETION IS THE BEST MEDICINE!