ASPHYXIA NEONATORUM (1).pptx
- 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. DEFINITION WHO NNPD AAP
- 4. 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 period
- 5. DEFINITION ANOXIA - complete lack of oxygen as a result of a number of primary causes HYPOXIA -decreased arterial concentration of oxygen leading to tissue anoxia ISCHEMIA refers to blood flow to cells or organs that is insufficient to maintain their normal function
- 6. INCIDENCE THE FREQUENCY OF PERINATAL HYPOXIA IS APPROXIMATELY 1% TO 1.5% in the west INVERSELY RELATED TO BIRTH WEIGHT &GESTATIONAL AGE O.5%OF LIVE BORN INFANTS >35 WEEKS ACCOUNTS FOR 20% OF PERINATAL DEATHS
- 7. FACTORS Mat. Oxygenation Blo Blood flow mother to placenta Blood flow placenta to fetus Gas Exchange across placenta or fetal tissue Fetal O2 Req.
- 8. PATHOPHYSIOLOGY Hypoxia Diving seal reflex Shunting of blood to brain adrenals & heart Away from lungs, kidney gut & skin NON BRAIN ORGAN INJURY Shunting of blood to brain adrenals & heart
- 9. Shunting of blood to brain adrenals & heart
- 10. PATHOPHYSIOLOGYBRIEF ASPHYXIA TRANSIENT INCREASE AND THEN DECREASE OF <HR> MILD ELEVATION IN <BP> INCREASE IN <CVP> NO CHANGE IN <CO> DIVING REFLEX REDISTRIBUTION OF<CO> BRAIN HEART ADRENALS
- 11. PROLONGED ASPHYXIA CEREBRAL BLOOD FLOW BECOMES DEPENDENT ON SYSTEMIC BLOOD FLOW LOSS OF CEREBROVASCULAR AUTOREGULATION HYPOTENSION DECREASED CEREBRAL BLOOD FLOW ANAEROBIC METABOLISM INTRACELLULAR ENERGY FAILURE{due to increased utilisation of glucose in the brain } FALL IN THE CONCENTRATION OF GLYCOGEN PHOSPHOCREATINE ATP
- 12. PATHOGENESIS OF HYPOXIC ISCHEMIC BRAIN INJURY ADENOSINE •HYPOXANTHINE XO •XANTHINE O2 FREE RADICALS DECREASED ATP •GLUTAMATE RELEASE NMDA RECEDPTOR •INTRACELLULAR Ca activates lipase •FREE FATTY ACIDS,arachadonic acis o2 •Free radicals INCREASED LACTATE •ANAEROBIC METABOLISM •HYPOGLYCEMIA DUE TO LOSS OF STORES
- 13. CELLULAR CHANGES DIMINISHED OXIDATIVE PHOSPHORYLATION AND ATP PRODUCTION ENERGY FAILURE IMPAIRS ION PUMP FUNCTION ACCUMULATION OF INTRACELLULAR Na,Cl,H2O& Ca EXTRACELLULAR K EAA eg.GLUTAMATE
- 14. • INTRACELLULAR OSMOTIC OVERLOAD OF Na and Ca • EXCESSIVE EAA ACTING ON NMDA RECEPTORS IMMEDIATE NEURONAL DEATH • UNCONTROLLED ACTIVATION OF ENZYMESAND SECONDARY MESSENGERS eg. Calcuim dependend lipases,proteases,caspases • PERTUBATION OF MITICHONDRIAL RESPIRATORY ETC • GENERATION OF FREE RADICALS AND LT • GENERATION OF NO THROUGH NO SYNTHETASE • DEPLETION OF ENERGY STORES DELAYED NEURONAL DEATH
- 15. REPERFUSION INJURY REPERFUSION OF PREVIOUSLY ISCHEMIC TISSUE MAY CAUSE INJURY AS IT CAN PROMOTE FORMATION OF EXCESS REACTIVE O2 SPECIES Eg. SUPEROXIDE,HYDROGEN PEROXIDE,HYDROXYL,SINGLET O2 ACTIVATE ENDGENOUS SCVENGER MECHANISM DAMAGE TO CELLULAR PROTEINS LIPIDS AND NUCLEIC ACIDS DAMAGE TO BBB INFLUX OF NEUTROPHILS RELEASE OF INJURIOUS CYTOKINS- IL I B,TNF ALPHA, MICROGLIA
- 16. NEUROPATHOLOGY OF PERINATAL ASPHYXIA • HIE • NECROSIS OF BRAINSTEM NUCLEI • SAH TERM NEWBORN • PERIVENTRICULAR HAEMORRAGIC INFARTION • PERIVENTRICULAR IV BLEED • PERIVENTRICULSR LEUCOMALACIA PRETERM NEWBORN
- 17. SYSTEMIC EFFECTS OF ASPHYXIA CNS ……. HIE,SEIZURES,ICH,INFARTS,CEREBRAL EDEMA,HYPOTONIA,HYPERTONIA CVS …… MI ,TR,POOR CONTRACTILITY,HYPOTENSION RENAL …… ATN OR CORTICAL NECROSIS ADRENAL …… HEMORRAGE
- 18. GI …… PERFORATION,ULCERATION WITH HAEMORRAGE AND NECROSIS METABOLIC…… ADH, HYPONATREMIA,HYPOGLYCEMIA,HYPOCALCEMI A, MYOGLOBINUREA HEMATOLOGICAL …… DIC INTEGUMENT …… SUBCUTANEOUS FAT NECROSIS
- 19. INTRODUCTION PERINATAL ASPHYXIA impaired gas exchange PERSISTENT FETAL HYPOXIA AND HYPERCARBIA {estimated by fetal acidosis UMBELICAL ARTERY p H < 7.0}
- 20. AT RISK INFANTS NEONATAL DEPRESSION: prolonged transition from INTRA to EXTRA uterine life WITH f/s/o FETOMATERNAL COMPROMISE-CORD ROUND NECK NRNST BABY BORN THROUGH MECONIUM STAINED LIQOUR SUGGESTIVE OF INTRAUTERINE STRESS DIABETIC OR TOXEMIC mother IUGR BREECH POST DATED
- 21. ETIOLOGY Intrapartum or Antepartum (90%) Placental Insufficiency Post partum (10%) Pulmonary Cardiovascular Neurologic Insufficiency
- 22. SPECIFIC MANAGEMENT PREVENT FURTHER BRAIN DAMAGE Maintain temperature, perfusion, oxygenation & ventilation Correct & maintain normal metabolic & acid base milieu Prompt management of complications
- 23. 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
- 24. SUPPORTIVE CARE T - Temperature A - Airway B - Breathing C - Circulation F - Fluid M - Medications F - Feed M - Monitoring C - Communication F - Followup
- 25. SUBSEQUENT MANAGEMENT Oxygenation & ventilation Adequate perfusion Normal glucose & calcium Normal hematocrit Treat seizure
- 26. 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
- 27. 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.
- 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. IMPACT BRAIN INJURY THAT OCCURS IN THE PERINATAL PERIOD IS ONE OF THE MOST COMMON RECOGNISABLE CAUSES OF SEVERE LONG TERM SEQUELAE… {NEUROLOGICAL DEFICITS IN CHILDREN OFTEN REFFERED TO AS CEREBRAL PALSY}
- 30. HYPOXIC ISCHEMIC ENCEPHALOPATHY FULFILLING CRITERIA 1)APGAR<3@ >5min 2)fetal heart rate <60beats/min 3)prolonged >1hr acidosis 4)seizures within 24 to 48 hrs 5)burst suppression pattern on eeg
- 31. PATHOLOGY DEPENDENT ON AFFECTED ORGAN AND SEVERITY COAGULATION NECROSIS AND CELL DEATH CONGESTION AND PETICHIAE SEEN IN PERICARDUIN PLEURA THYMUS HEART ADRENALS AND MENINGES PULMONARY ARTERY SMOOTH MS HYPERTROPHIES LEADING TO PULMONARY HTN PROLONGED IU HYPOXIA INADEQUATE PERFUSION OF WHITE MATTER PVL
- 32. CEREBRAL BLOOD FLOW ASSESMENT XENON CLEARENCE TECHNIQUE JUGULAR VENOUS OCCLUSION PLETHISMOGRAPHY mean cerebral blood flow=50-60ml/min/100g brain wt…..in asphysiated term babies it is one half of normal at 2 days and remains decreased for 4 days ,cbf of 20ml/min/100mg in term or preterm results in permanent brain damage NONINVASIVE DOPPLER pulsatility index =( systolic amplitude – diastolic amplitude)/systolic amplitude ….normal in mildly asphysiated and and low in severe asphyxia
- 33. PRINCIPLES OF PATHOPHYSIOILOGY USED IN MANAGEMENT • CO ORDINATE WITH OBSTRETRIC TEAM • NEWBORN RESUCITATION IDENTIFICATION OF HIGH RISK INFANT • VENTILLATION MAINTAIN p CO2WITHIN NORMAL RANGE(STEAL PHENOMENON HYPERCAPNIA,HYPOCAPNIA DECREASES CBF) • Perfusion promptly treat hypotension avoid hypertension • Fluid status initial fluid restriction follow serum sodium and daily weight • Blood glucose maintain within normal levels • Seizures treat wit eeg corelates • Electrolyte imbalance monitor calcium magnesuim and electrolytes • Infection lp in suspected cases of cns infection SUPPORTIV E CARE • Hypothermia…selective cooling to 2-4 degree celcius reduce incidence if tissue damage • O2 free radical scavenger,inhibitors • Eaa antagonists • Prevention of no formation • Ca channel blockers POTTENTIAL NEUROPROTECTIVE STRATEGIES…AMEILORATING SECONDARY BRAIN DAMAGE
- 34. BIBILIOGRAPHY MANUAL OF NEONATAL CARE CLOHARTY 6TH EDITION NELSON TEXTBOOK OF PAEDIATRICS 18TH EDIYION NEUROLOGY OF THE NEWBORN VOLPE4TH EDITION NEONATAL NEUROLOGY GERALD M FENICHEL 3RD EDITION RECENT ADVANCES IN PAEDIATRICS EDITED BY T.J.DAVID 18
- 35. THANK YOU
- 36. Pathophysiology Within minutes of onset of fetal hypoxia : Bradycardia Hypotension Decreased cardic output Severe metabolic as well as respiratory acidosis
- 37. Initial circulatory response of the fetus Increased shunting through the ductus venosus,ductus arteriosus and foramen ovale