Perinatal Asphyxia

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Perinatal Asphyxia

  1. 1. Perinatal Asphyxia Dr. Kalpana Malla MD Pediatrics Manipal Teaching HospitalDownload more documents and slide shows on The Medical Post [ www.themedicalpost.net ]
  2. 2. PERINATAL ASPHYXIADefinition An insult to the fetus or newborn due to lack ofoxygen (hypoxia) and /or lack of perfusion (ischemia) to various organs.Associated with Tissue lactic acidosis • Hypoventilation • Hypercapnea 2
  3. 3. PERINATAL ASPHYXIAIncidence1-1.5%20% of perinatal deathsIncreased risk in IDM Toxemic mothers IUGR Breech Postmature 3
  4. 4. SEQUENCE OF EVENTS HR…..decrease BP…...decreaseNormal Resp...Rapid breathing….Pr.Apnea….Irreg.breathing…Sec.Apnea Resuscitation Resuscitation Normal Respiration Normal Respiration 4
  5. 5. ETIOLOGY 90% Antepartum/ Intrapartum 10% Postpartum FACTORSMaternal:- Hypertension- chronic / pre-eclampsia - Diabetes, anemia,, malnutrition - Hypoxia-Pulmonary/Cardiac/ - heart Ds, Bronchial asthma 5
  6. 6. FACTORSMaternal……:HypotensionIntrauterine infectionsProlonged and difficult 2nd stage of labourPlacental: Infarction/fibrosis/abruptionCord Accidents: Prolapse / True knots / compression/Abn. vessels
  7. 7. FACTORSFetal:• Infection - intrauterine• Anemia - Feto-fetal or feto maternal transfusion• IUGR/ Postmaturity - Meconium aspiration tracheal plug by blood mucus• Cong malformations - choanal atresia, laryngeal web,D. hernia, TEF,ICH• Hydrops fetalis
  8. 8. PATHOPHYSIOLOGYDiving reflex: Shunting of blood to brain ,heart, adrenals andaway from gut, kidney, liver, spleen ,skeletalmuscle and skinProgressive asphyxia: Hypoxia, Hypercapnea, acidosis Pulmonary vasoconstriction, R to L shunt Decrease in HR, CO, BP Cerebral edema- Petechial hemorrhage, SIADH, Na- intracellular accumulation 8
  9. 9. TARGET ORGAN-BRAIN HIE:PATHOPHYSIOLOGYHypoxia Alteration in glucose and energymetabolism loss of autoregulation & decreasedcardiac function ischemiaSevere hypoxia and ischemia failure of oxidativephosphorylation & ATP productionAccumulation of Na, Cl,Ca intracellular and K andexcitatory neurotransmitters extracellularneuronal death 9
  10. 10. HIE- PATHOLOGY1. Selective neuronal necrosis - Cerebral and cerebellar cortex, Thalamus, brain stemnuclei2. Focal and multifocal cortical necrosis3. Watershed infarct4. Parasagittal cerebral injury5. Periventricular leucomalacia6. Status murmoratus. 10
  11. 11. Hypoxic Ischaemic Encephalopathy• Most important consequence of perinatal asphyxia• Hypoxic ischaemic insult to the brain• 25-30% of survivors have permanent damage like CP and MR.• 15-20% with HIE die
  12. 12. SARNAT STAGINGFeatures Stage1 Stage 2 Stage3 Mild Moderate Severe1.Level of Hyperalert Lethargic Stuperous consciousness Irritable Obtunded Comatose2.Neuromuscular control. Muscle tone N Hypotonia Flaccid Posture N Flexion Decerebration Reflexes   Decreased / Absent3. Reflexes Suck Weak Weak /Absent Absent Moro Strong Weak Absent 12
  13. 13. SARNAT STAGINGFeatures Stagee1 Stage 2 Stage3 Mild Moderate Severe4.Autonomic Gen.sympathetic Gen.Parasymp Both depressed function Pupil Mydriasis Miosis Midposition Resp Spont Spont Periodic,apnea HR Tachycardia bradycardia Variable5.Seizures None common Uncommon6.EEG Normal abnormal abnormal7. Duration <24hr 24hr-14day Day-weeks8.Outcome Good Variable Death
  14. 14. SARNAT STAGINGFeatures Stage1(Mild) Stage 2(Moderate) Stage3(Severe)4.Autonomic Gen.sympathetic Gen.Parasymp Both depressed function Pupil Mydriasis Miosis Midposition Resp Spont Spont Periodic,apnea HR Tachycardia bradycardia Variable5.Seizures None common Uncommon6.EEG Normal abnormal abnormal7. Duration <24hr 24hr-14day Day-weeks8.Outcome Good Variable Death
  15. 15. APGAR SCORE APGAR Score: 8-10 No asphyxia 5-7 Mild asphyxia 3-4 Moderate asphyxia 0-2 Severe asphyxia Virginia Apgar 0_________ 1__________ 2_____Heart rate 0 <100 >100Respiration 0 weak, irregular good cryReaction 0 slight goodColour blue or pale body pink limbs blue all pinkTone limp some movement active movements limbs well flexed
  16. 16. ASSESSMENT/PRECAUTIONSPerinatal1.Awareness of problems and high risk2.Fetal movement count3.Fetal BPP5. Monitor FHR6.Progress of labor7.Fetal scalp -pH8.Presence of meconium 16
  17. 17. SYSTEMIC MANIFESTATIONSBrain(28%)- HIE, ICH, Apneic attacks, SeizuresHeart(25%)- PFC, Arrhythmia, Myocardial damage,TR,CCFLungs(23%)- Meconium aspiration, Pul.hemorrhage Pneumothorax, pneumoniaKidney(50%)- Hematuria, ARF, ATN, RVTGIT- NEC, Paralytic ileus 17
  18. 18. SYSTEMIC MANIFESTATIONS• Hematologic- DIC, Hyperbilirubinemia, sepsis• Endocrine- SIADH, Adrenal hemorrhage• Metabolic- hypoglycemia, hypocalcemia, hyperbilirubinemia
  19. 19. Late effects• Microcephaly• MR• Developmental delay• Cerebral palsy• Epilepsy• Visual, hearing impairement• Behavioral disturbances
  20. 20. MANAGEMENT• Ventilation-For hypoxia and hypercapnea• Maintain cerebral perfusion• Correction of hypoglycemia and hypocalcemia• Temperature maintenance• Control of seizure- Anticonvulsants• Cardiac effects-Ionotropes• Renal effects- Dopamine 21
  21. 21. CLINICAL MANIFESTATIONS OF NEUROLOGICAL SEQUELAE• Cerebral Palsy- Spastic diplegia, Spastic quadriplegia, Spastic hemiplegia Dystonic Choreo athetotic• Mental retardation• Epilepsy• Auditory, visual and language difficulties 22
  22. 22. PROGNOSIS• Overall mortality - 10-20%• Neurological sequele - 20-45%• Sarnat Stages 1- 100% Normal neurological outcome 2- 80% Normal neurological outcome 3- 50% deaths, 50% major neurological sequelae• Risk for CP - 5-10%• Subtle school problems in neurologically and mentally normal survivors of HIE stage 1-nil, stage 2- 18-35% 23
  23. 23. Thank youDownload more documents and slide shows on The Medical Post [ www.themedicalpost.net ]

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